phd clinical trials london

PhD studentships in clinical trials and methodology

10 Feb 2022

We currently have opportunities to apply for fully-funded PhD studentships based at the MRC Clinical Trials Unit. Our students undertake research that aims to improve patient care by improving the way in which the healthcare evidence base is developed, often linked to current or recent clinical trials and supported by staff within the Unit. Our projects span a variety of topics related to improving clinical trials and the health of society including:

• Improving how clinical trials are conducted
• Developing new existing clinical trial designs
• Identifying better ways to analyses clinical trial data
• Understanding how the results of clinical trials can best inform practice
• Expanding evidence synthesis techniques to make the most of clinical trial data

Successful applicants, who will enrol in September 2022, will be funded at current MRC rates for 3 years, including tuition fees at the UK student rate, a Research Training and Support Grant (RTSG) and stipend (to include London Weighting). Overseas students are eligible to apply for additional funding to cover overseas fees.  

Further information:

• Details of available projects and how to apply

Pragmatic Clinical Trials Unit

Phd opportunities.

Here are some exciting ideas for PhD projects to develop, supervised by leading experts in pragmatic trials. However, if you have an idea that is not listed below, please feel free to contact us on [email protected] and we will be happy to consider other ideas.

Potential projects:

1. Optimal incomplete stepped wedge trials: staircase designs and beyond (Dr Richard Hooper)

2. Design of stepped wedge trials with continuous recruitment (Dr Richard Hooper)

3. Effectiveness and cost-effectiveness of interventions to improve uptake and adherence to cardiovascular prevention treatments (Professor Borislava Mihaylova)

4. Impact of asthma on health outcomes, healthcare use and costs (Professor Borislava Mihaylova)

5. Use of routine healthcare data to develop long-term disease models for management of asthma (Professor Borislava Mihaylova)

6. Assessing effects of interventions on socioeconomic inequalities to inform health policy (Professor Borislava Mihaylova)

7. Evaluating cost-effectiveness of complex health interventions (Professor Borislava Mihaylova)

8. Efficiency of Trials within Cohorts designs (Dr Clare Relton)

9. Opt-out consent for pragmatic trials within primary care (Dr Clare Relton)

11. What are the barriers for the inclusion of studies within pragmatic trials and how to overcome them (Dr Clare Relton)

12. Effective ways to create prediction models of recruitment rate for pragmatic trials???

16. Investigation of childhood conditions (respiratory diseases, mental health conditions, etc.), family relations and well-being indicators later in life using cohort data (such as the National Child Development Study) (Dr Florian Tomini)

17. Health and socioeconomic impact of (work-related) asthma and respiratory conditions using the UK labour force survey (Dr Florian Tomini)

18. The impact of financial incentives design on inequality for mental health patients in England (Dr Yan Feng)

21. Using routinely collected data - methods and pitfalls (Professor Sandra Eldridge)

22. Analysing trials with ordinal outcomes and clustering in one arm (Professor Sandra Eldridge)

23. Informed consent in trials within cohorts and cluster randomised trials (Professor Sandra Eldridge and Dr Clare Relton)

24. Synthesising information from pilot and feasibility studies (Professor Sandra Eldridge)

25. Bias in pragmatic trials (Professor Sandra Eldridge)

King's College London

Doctorate in clinical psychology dclinpsy.

Key information

The three-year, full-time Doctorate in Clinical Psychology is based within the Institute of Psychiatry, Psychology and Neuroscience (IoPPN). Trainees spend three days a week on supervised clinical practice placements and two days a week are dedicated to teaching, study and research.

Aims & philosophy

To benefit service users, carers and wider society by training clinical psychologists who:

• are skilled in evidence-based psychological assessment and intervention
• produce applied research of the highest quality and impact
• progress to become leaders within the NHS, clinical academia and beyond

The training programme values the reflective scientist-practitioner model as a basis for clinical psychology. There is a strong emphasis on integration of theory, research and practice in all aspects of the programme.

The biopsychosocial framework underpinning the Programme identifies biological, psychological and social factors that contribute to the development and maintenance of psychological difficulties and mental disorders across the lifespan. Our understanding of the framework is that it is linked to a continuum view of psychological difficulty. Thus, the programme seeks to understand these difficulties from an assumption of commonality of experience and human potential to support wellness and resilience.

The programme takes cognitive-behavioural therapy (CBT) as its primary therapeutic modality, reflecting the world-leading research expertise within the IoPPN and its evidence base. Family therapy/systemic practice is the second therapeutic modality.

The Programme is based predominantly within King's Health Partners (an Academic Health Sciences Centre) which comprise King's College London and three of the highest rated NHS Foundation Trusts in the country: South London and Maudsley, King's College Hospital, and Guy's and St Thomas'. A particular strength of the programme is the cohesive and comprehensive range of local and national specialist placement opportunities across these trusts and other placement services. In line with the goals of the NHS long term plan, placements offer trainees opportunities to work in local clinical pathways improving access to services for people from our diverse local communities.

The IoPPN DClinPsy Training Programme is committed to the principle of equality of opportunity for all trainees and staff. The Programme values and positively promotes equality, inclusion and diversity. At the IoPPN and local Trusts, there is much expertise relating to Culture, Equality, Diversity and Inclusion (CDI) in clinical, research, and teaching activities.

Additional information

The programme meets the Health and Care Professions Council (HCPC) education and training standards – the statutory regulator for practitioner psychologists in the UK, and has full accreditation from the British Psychological Society (BPS).

The course is also accredited by the British Association for Behavioural and Cognitive Psychotherapies (BABCP) – Level 1 (for all trainees) and Level 2 (for a subset of trainees), alongside the Association of Family Therapy and Systemic Practice (AFT) – Foundation Level (for all trainees).

On successful completion of the programme trainees are awarded the Doctorate in Clinical Psychology. The award confers eligibility to apply for registration with the HCPC to practise as a clinical psychologist in the UK, and graduates are able to apply for full membership of the Division of Clinical Psychology from the BPS.

Trainees are full-time professionals in the NHS, registered students at King's College London and key stakeholders whilst training. Throughout the training programme, trainees are encouraged to synthesise and reflect on different aspects of their learning and work as part of their professional development and integration of their personal and professional aspects. Key contributors to this process are the use of clinical supervision, discussions in teaching workshops, meetings with personal tutors and appraisers, and reflections in their logbook and clinical assessments.

Trainees help to shape the Programme's development and evolution through representation and participation in the majority of the Programme committees. There are also a number of opportunities for trainees to begin working as partners and leaders whilst training via involvement in working parties and groups focused on priorities within clinical psychology training.

The Programme has a number of support systems in place to help ensure that trainees are well supported and to create a stimulating and rewarding environment for trainees to develop personally and professionally during their training.

• Before joining the Programme, each new trainee is contacted by their ‘buddy’ (one of the current first year trainees) to facilitate their transition onto the Programme.
• Trainees will be line managed by a Clinical Director on the Programme
• Each trainee is allocated a personal support tutor and mentor – a qualified clinical psychologist available for confidential advice and support who is available to meet at least once per term throughout training. The personal support tutor, where possible, is matched to trainee career interests to allow for mentoring alongside pastoral support.
• Each trainee is also allocated a clinical tutor who will visit them on placement throughout the three years to maximise continuity, support and development.
• Each trainee is allocated an appraiser from within the Programme team to support progression across all aspects of the Programme.
• Each trainee is allocated a research tutor from the Programme team to support them with any questions or concerns about any aspect of their research.
• Reflective practice groups and themed reflective case discussions run throughout training, which provide an opportunity for trainees to reflect on training and the impact of clinical work.
• Dedicated reflective spaces are offered to trainees from racially and ethnically minoritised (REM) backgrounds. These spaces aim to offer support in a safe environment.
• Trainees’ identifying as White will be invited to attend a dedicated reflective space to consider the impact of their identity in training.
• A support group is available for trainees with childcare responsibilities, which includes drop-in meetings with clinical tutors.
• Orientation meetings are scheduled in the timetable to facilitate transition into the following year of study. At the end of the final year there is an exit meeting to allow trainees to reflect with the Programme Team about their experiences of the training programme.
• Trainees with disability support needs can book a confidential appointment with a Disability Adviser at King’s College London Disability Support . This will help develop an Inclusion Plan which summaries aspects your disability and provides recommendations of support strategies to ensure we can best support you throughout your training experience.

As a course, we care about the psychological well-being of our trainees and aim to ensure we can best support trainees who may be experiencing difficulties or have additional support needs. We recognise that whilst training you are likely to experience periods of increased stress given the various pressures that need to be managed across different components of the course, as well as any additional stressors including physical and mental health concerns, or other personal factors that may impact on well-being. We have a number of sources of support available to our trainees as well as resources and signposting of services.

• How to apply
• Fees or Funding

UK tuition fees

Home applicants who meet the above entry requirements criteria are eligible for an NHS funded place and are not required to pay tuition fees.

International tuition fees 2023/24

Full time tuition fees: £31,260 per year

International tuition fees 2024/25

Full time tuition fees: £33,450 per year

These tuition fees may be subject to additional increases in subsequent years of study, in line with King’s terms and conditions.

If you receive an offer for this programme, you will be required to pay a non-refundable deposit to secure your place. Deposit payments are credited towards the total tuition fee payment.

The International deposit is £2000.

• If you receive an offer before March, payment is due by 20 March.
• If you receive an offer between 1 March and 20 May, payment is due within one month of receiving the offer.
• If you receive an offer between 21 May and 15 July, payment is due within two weeks of receiving the offer.
• If you receive an offer between 16 July and 15 August, payment is due within one week of receiving the offer.
• If you receive an offer from 16 August onwards, payment is due within three days of receiving the offer.

If you are a current King’s student in receipt of the King's Living Bursary you are not required to pay a deposit to secure your place on the programme. Please note, this will not change the total fees payable for your chosen programme.

Please visit our web pages on fees and funding for more information.

• Study environment

Base campus

Denmark Hill Campus

Home to the Institute of Psychiatry, Psychology & Neuroscience

The Doctorate is intensive, running for three years full-time. The programme consists of academic, clinical and research components, and trainees are required to pass in all areas..

Academic teaching, research supervision and clinical supervision are mainly carried out by members of the Department of Psychology or other departments within the Institute of Psychiatry, or by clinical psychologists working within King's Health Partners, giving the programme an overall cohesion and sense of community. The Programme also receives specialist contributions to its academic teaching from invited outside speakers and experts.

For departmental and Institute research interests visit the IoPPN webpages.

In each year, trainees spend three days per week on supervised clinical placements (Tuesdays to Thursdays, 9:00 – 17:00) with Mondays and Fridays dedicated to teaching and research. Trainees undertake six 6-month placements. The four ‘core’ areas of the programme are Adult and Child Mental Health, (year 1) and Older Adults and Intellectual Disability (year 2). The third year comprises two specialist or supplementary placements.

Attendance at all course components is mandatory. Trainees are also expected to undertake their own independent learning.

The length of the Programme cannot be reduced through the accreditation of prior learning or experience. All trainees are required to complete the full Programme of training in order to qualify and while on the Programme, all trainees take annual holiday entitlement within set time periods to fit in with teaching and placement attendance requirements.

Academic curriculum

The curriculum comprises of teaching streams that are led by academic clinicians and NHS service-based specialist clinicians. This curriculum is revised through consultation processes with NHS specialists, trainees, service users and NHS commissioners. A foundational theme that sits across all the teaching streams is that of culture, diversity, equality, and inclusion. The specific teaching streams fall under the following headings:

• CBT Fundamentals
• Adult General
• Adult Addictions
• Adult Anxiety
• Adult Forensic
• Adult Psychosis
• Clinical Health Psychology
• Clinical Skills
• Clinical Neuropsychology
• Culture, Equality, Diversity & Inclusion
• Family Therapy
• Intellectual Disability & Neurodevelopmental Disorders
• Additional Therapy Approaches
• Professional Issues
• Reflective Practice & Reflective Case Discussions
• Research, Assessment and Methodology
• Supervision

The programme delivers teaching based on research, theoretical literature, practice-based experience and lived experience (expert by experience and carer input). Teaching is provided in lectures, workshops, seminars and tutorials. Methods of delivery include, discussions, polls, case examples, role-plays, video displays, and didactic teaching. This is designed according to the material to be covered and the stage of training. Trainees are encouraged to contribute to the process; significant aspects of learning and development will come from each other.

Clinical practice placements

Trainees undertake six 6-month placements. The four ‘core' areas of the programme are Adult and Child mental health (year 1) and Older adults and Intellectual disability (year 2); the third year comprises two specialist or supplementary placements. The majority of placements are located within South London and are accessible via public transport links. Trainees prior experience and future career preferences are taken into consideration in placement allocation.

The third year comprises two specialist or supplementary placements. There is a wide, exciting range of specialist placement opportunities for trainees to choose from, at South London and Maudsley NHS Foundation Trust (SLaM), King’s College Hospital NHS Foundation Trust (KCH), Guy’s and St Thomas’ Hospital NHS Foundation Trust (GSTT) and in other organisations. SLaM provides the widest range of NHS mental health services in the UK.

Placements are offered in a variety of specialisms and settings, including primary care, secondary care, inpatient, secure settings and non-statutory organisations. We are fortunate to have many national services across the Trusts, meaning that trainees have access to a number of specialist placements. Placements may be based in the community or hospital settings.

By May of the final year, trainees are required to submit a doctoral level research thesis of between 25,000 to 55,000 words.

The thesis is comprised of:

• Service-Related Project
• Empirical Project
• Systematic Review

The Service-Related Project is completed in the first year, supervised by a clinical placement supervisor. Trainees gain experience of conducting an NHS-related project that will inform service development. Recent projects have directly investigated issues of equality and diversity in service provision.

The Empirical Project and Systematic Literature Review are completed in the second and third year, supervised by a main and second supervisor. Staff in the Department of Psychology and wider Institute of Psychiatry, Psychology and Neuroscience offer research expertise and supervision in a wide range of clinical topics. Most trainees are able to choose their research topic based on their interests and learning needs, and to co-create a research project with their supervisors. Trainee research is supported by the rich research environment at King’s, including close links with the department of Biostatistics & Health Informatics.

A developmental, competency-based approach is taken to assessment, combining formative and summative assessment methods. Please note that a number of the summative assessments undertaken by trainees in the third of training will be dependent on their pathway (either BABCP Level 2 or AFT Intermediate).

The failure of two placements, or of an examination resit, or resubmitted/resat case studies, case conferences or assessments of clinical competence, or the viva examination, will constitute a Programme failure. No lesser exit award is available under the Programme.

Summative Assessments (all trainees)

• Qualifying examinations are held in June of the first year. The pass mark is 50% and trainees who fail are allowed to re-sit on one occasion in August.
• Case Conferences : In the first year of training, trainees are asked to present a case that demonstrates their CBT knowledge and skills. In the second year of training, trainees are asked to present a case where they have worked with more than one person in the room, and to offer a systemic formulation and treatment plan to assess their knowledge and skills in systemic practice.
• Case Studies : Early in the second year of training, trainees will need to submit a CBT case study that will demonstrate theory practice links and reflection on their learning and development as CBT therapists.
• All six practice placements are graded Pass/Fail by placement supervisors.
• The research thesis is assessed at a viva by two external examiners.
• Research Progress Report trainees submit a report on their research progress every 6 months, which is formally reviewed by their supervisor and a panel of research tutors; a satisfactory outcome of the review is required for progression.

Head of group/division

Professor Katharine Rimes

Contact for information

Kayleigh Rawlings, Programme Coordinator

[email protected]

Important Information:

Before contacting the programme, please note we are unable to offer individual advice on how to create a successful application or advise on what route applicants should take. There are many different routes onto the Doctorate, therefore the pathway undertaken should be the applicant’s choice, based on their interests and career aims.

Contact email

Further resources:

• DClinPsy Clearing House Profile
• KCL-DClinPsy information about applying (padlet.org)
• Twitter: @KingsDClinPsy
• Entry requirements

Find a supervisor

Search through a list of available supervisors.

Accommodation

Discover your accommodation options and explore our residences.

Connect with a King’s Advisor

Want to know more about studying at King's? We're here to help.

Learning in London

King's is right in the heart of the capital.

London School of Hygiene & Tropical Medicine

Clinical trials by distance learning, (certificate, diploma and msc).

From managing heart failure to supporting people with HIV, clinical trials make a difference to communities across the globe. Discover our research in this area and learn to carry out trials effectively.

Study Clinical Trials and develop the skills to save lives and shape the future of health. We were one of first universities in the UK to create a distance learning programme focused on clinical trials. With extensive expertise in this area and academics in every corner of the globe, we’ll share best practices for carrying out research that tests drugs, comparing alternative treatments, and using cutting-edge methods.

Your award will depend on the number of modules you complete. We offer this distance learning programme as a Certificate, Diploma and MSc.

What you will learn

• Explore the issues involved in the design, conduct, analysis and interpretation of randomised controlled trials of health interventions
• Understand what happens before a trial – review the literature to see what’s been done before and whether it’s reliable
• Practise reporting your findings in a way that is transparent, accurate and helps others apply your results to the real world
• Become confident handling statistics for clinical trials
• Pick optional modules to expand your interests in this area or choose topics from other areas of specialism in the School
• Develop the skills you need to excel in your clinical trials career and make a difference to people’s lives globally

The aims and learning outcomes are detailed in the  programme specification .

It’s not just students that are based globally. Our teaching team are too, working on projects that are supporting the health of people around the world. For example, some have studied the management of heart failure and influenced the UK National Institute for Health and Clinical Excellence guidelines, while others have helped develop maternal and child health programmes in India.

We’ve designed this course to help you look at all the aspects that influence clinical trials in practice. You’ll get support in everything from reviewing the literature effectively to analysing statistics so you can feel confident making conclusions and reporting key findings.

Once you complete the core modules, you have the option to apply for the blended learning option to study up to two modules on-campus in London. This is a fantastic opportunity to meet other students and tutors in person; and engage in face-to-face discussion-based learning.

Who is it for?

Because this programme is distance learning, students join us from across the globe. Wherever you’re living in the world, the content will be relevant to you – whether you are working in a low-, middle- or high-income country.

Many of our students are working in this area already and are eager to take their skills to the next level. If that describes you, we’ll help you expand your role in the design, management, analysis and reporting of clinical trials.

You’ll learn at your own pace and study when it suits you. The course can be completed in two years, but you can spend up to five years studying with us. We run live sessions regularly which we encourage you to join if you can. These are run at two different times in the day so you can pick the one that works with your time zone.

• Programme specification

Related courses

We also offer an  Essentials of Clinical Trials  short course.

Watch Programme Director Claire Snowdon talks how clinical Trials are essential in finding solutions to many health care problems around the world. 

"LSHTM manages to cultivate a really rewarding sense of achievement through distance learning. You feel engaged with the course, and the modules are really challenging and interesting."

The below structure outlines the proposed modules for this programme. Programme and module specifications provide full details about the aims and objectives of each module, what you will study, what materials are provided and how the module is assessed.

• Programme regulations
• Module specifications
• Clinical Trials - suggested schedules
• Postgraduate Certificate: 4 compulsory core modules 
• Postgraduate Diploma: 8 modules (4 compulsory core + 4 elective modules * ) 
• Master’s: 11 modules (4 compulsory core + 5 elective* + 2 compulsory modules † ) 

*For the PG Diploma and MSc elective modules, at least three modules must be taken from selection group CTM2 or two elective CTM2 modules selected from a list of options and EPM101 Fundamentals of Epidemiology. The remaining module(s) can be chosen from CTM2 or the other selection groups. 

†MSc students must take CTM201 Protocol Development and complete the CTM210 Integrating Module, comprising a written report, usually in their final year of study. 

It is possible to register for the PG Certificate in the first instance then, on successful completion of the compulsory core modules, transfer your registration to the PG Diploma or MSc.

The majority of modules listed below are also available to study as individual modules .

• CTM101 Fundamentals of Clinical Trials
• CTM102 Basic Statistics for Clinical Trials
• CTM103 Clinical Trials in Practice
• CTM104 Reporting and Reviewing Clinical Trials

Clinical Trials elective modules (CTM2):

• CTM201 Protocol Development (compulsory for the MSc, elective for the PG Diploma)
• CTM202 Trial Designs
• CTM203 Project Management and Research Co-ordination
• CTM204 Regulatory affairs, Good Clinical Practice and Ethics
• CTM205 Data Management
• CTM206 Data Monitoring and Interim Analyses
• CTM208 Further Statistical Methods in Clinical Trials
• CTM209 Cluster Randomised Trials
• CTM210 Integrating Module (compulsory for the MSc)

Recommended modules selection group:

• EPM101 Fundamentals of Epidemiology
• EPM301 Epidemiology of Infectious Diseases
• EPM302 Modelling and the Dynamics of Infectious Diseases
• EPM304 Advanced Statistical Methods in Epidemiology
• EPM307 Global Epidemiology of Non-Communicable Diseases
• GHM201 Health Systems
• IDM201 Bacterial Infections
• IDM202 Nutrition and Infection
• IDM203 Parasitology
• IDM204 Viral Infections
• IDM205 Healthcare-Associated Infection
• IDM213 Immunology of Infection and Vaccines
• IDM215 Water, Sanitation and Hygiene
• IDM301 Epidemiology and Control of Infectious Diseases
• IDM502 Tuberculosis
• IDM503 Malaria
• PHM201 Health Decision Science
• PHM203 Economic Analysis for Health Policy
• PHM204 Economic Evaluation
• PHM205 Environmental Epidemiology
• PHM206 Environmental Health Policy
• PHM207 Health Care Evaluation
• PHM209 Globalisation and Health
• PHM210 Managing Health Services
• PHM211 Medical Anthropology in Public Health
• PHM212 Organisational Management
• PHM213 Principles & Practice of Health Promotion
• PHM214 Conflict and Health
• PHM215 History and Health
• PHM216 Sexual Health
• PHM218 Applied Communicable Disease Control
• PHM219 Evaluation of Public Health Interventions

Students wishing to study a module not on the above recommended list should contact the programme team  for advice. Approval may be given at the discretion of the Programme Directors.

(Note that restrictions and pre-requisites may apply to some of the modules above. Not all elective modules will be available every year).

Assessment varies from module to module but includes written assignments, groupwork and written examinations. Some modules involve only one type of assessment. Other modules use a combination of assessments. Details are given in the module specifications.

Where modules involve written examinations, these will take place in June.

Credits will be awarded for all modules (15 credits each) and the integrating module (MSc only, 30 credits) if successfully completed. To successfully pass an award, the following credits must be gained:

• Postgraduate Certificate – 60 credits
• Postgraduate Diploma – 120 credits
• Master’s – 180 credits

After successful completion of a minimum number of core modules, PG Diploma and MSc students may also be eligible for the  blended learning option , which allows for the study of up to two modules only (from a restricted list) at LSHTM in London during the Spring or Summer terms  in place of  distance learning modules. Please note that these options, and the dates when the modules are held at LSHTM, are subject to change - full details will be sent to all distance learning students in July each year.

Changes to the programme

LSHTM will seek to deliver this programme in accordance with the description set out on this programme page. However, there may be situations in which it is desirable or necessary for LSHTM to make changes in course provision, either before or after registration. For further information, please see our page on changes to courses .

Study materials

Learning is via directed self-study against a detailed set of learning objectives for each module. All CTM modules are delivered solely online, with access to a range of study resources, discussion forums and online webinar discussion sessions via LSHTM’s virtual learning environment, Moodle.

Details of the study materials for each module can be found in the module specifications . Materials and resources may include:

• Computer Assisted Learning materials provided electronically through Moodle for self-directed study
• E-books and other recommended readings
• Real-time and recorded online sessions with module tutors on specific topics
• Self-assessed assignments (Formative Assignments and past examination questions) plus specimen answers
• Examiners’ reports for two years which include Assessed Assignment and examination questions and specimen answers

Students are strongly encouraged to participate in module-specific discussions on Moodle, and to make use of LSHTM’s online library resources.

Module tutors provide feedback for all students via the online discussion forums and offer individual feedback on submitted assignments. Tutorial support is available from the beginning of October through to the end of May.

Flexible study

We know that if you have a full-time job, family or other commitments, and wish to study at a distance, you will have many calls on your time. The course allows you to study independently, at a time and pace that suits you (subject to some course-specific deadlines) using the comprehensive study materials provided, with support available from academic staff. You have between 1-5 years in which to complete the Postgraduate Certificate, and between 2-5 years in which to complete the Postgraduate Diploma or the MSc. 

Once registered, you will be sent the learning materials for the module(s) you have chosen to study. Clinical Trials module materials are mostly delivered online. These materials will take you through a programme of directed self-study, and indicate how and where you can obtain supplementary study materials and access tutorial support to enhance your studies.

The study year runs from the beginning of October through to the June exams, during which time tutorial support is available. Those writing the Clinical Trials integrating report will also continue to have tutorial support over the summer. Deadlines for submission of coursework vary per course but are usually in March, May, August and September.

The fees below refer to the 2024/25 academic year. Fees are subject to annual review and may be paid in one of two ways:

Either: on initial registration, a single payment covering the programme registration fee and all module fees for the duration of the programme

Or: pay the initial programme registration fee, plus the fee for each module you are taking in the first year. Then, in subsequent years, you pay the fee for each new module you take.

Individual modules (taken on a stand-alone basis with no registration fee)

Blended learning fees (for distance learning students attending modules in London)

All fees must be paid in pounds sterling (GBP) directly to the University of London. The University of London accepts:

• Western Union - Quick Pay
• Credit/debit card (Visa, MasterCard, Maestro, Electron, JCB)
• Sterling banker's draft/cheque
• International money/postal order 

Further details are given on the  University of London website .

Other costs

In addition to the fees payable to the University of London, you should also budget for the fee charged by your local examination centre to cover its costs; this fee will vary.

Academic requirements

All applicants are required to have:

• either a first or second class honours degree, or the equivalent, from a university or other institution acceptable to the University of London, in a subject appropriate to the course; or
• an appropriate professional or technical qualification, together with at least three years’ relevant experience, which satisfies the University as a qualification equivalent to a second class honours degree. All applications in this category will be considered on an individual basis

Qualifications from around the world are accepted; for further guidance please see the University of London's  qualifications for entrance . Students who do not satisfy the entrance requirements may still be admitted at the discretion of LSHTM on the basis of their academic qualifications, work experience and references.

English language requirements

You need a high standard of English to study this programme. You will meet our language requirements if you have achieved one of the following within the past three years:

• IELTS :  7.0  overall, with  6.5  in the written test and  5.5  in listening, reading and speaking.
• TOEFL iBT :  100  overall, with  24+  in writing,  23 +  in speaking,  22+  in reading and  21+  in listening.
• Pearson Test (Academic) :  68  overall, with  62+  in writing and  59+  in listening, reading and speaking.
• Cambridge Certificate of Advanced English :  185  overall, with  176+  in writing and  169+  in listening.
• Duolingo : must achieve an overall score of at least 130.

Alternatively, you may satisfy the language requirements if you have at least  18 months  of education or work experience conducted in English.

If you do not meet these requirements but believe you can meet the standard, the University of London may also consider your application.

Computer requirements

You must have regular access to a computer (or mobile device*) with an internet connection to use the University of London website and the Student Portal. These are where your programme’s study resources are located. Through the Student Portal you can register as a student, enter exams and use your programme’s Virtual Learning Environment (VLE). The VLE provides you with electronic learning materials, access to the University of London Online Library, networking opportunities and other resources.

To get the most from your studies, your computer should have at least the following minimum specification:

• a web browser (the latest version of Firefox, Chrome or Internet Explorer). This must accept cookies and have JavaScript enabled
• screen resolution of 1024 x 768 or greater
• sufficient bandwidth to download documents/files of at least 50 MB

and the following applications installed:

• word processor that reads Microsoft Word format (.doc)
• Adobe, or other pdf reader

Some of the CD-ROMs and software provided for use with Epidemiology modules may not be fully compatible with Apple Mac computers.

*Full mobile access is not available for all programmes

Our distance learning programmes are run in collaboration with the University of London , a federation of 18 independent member institutions and universities, of which the London School of Hygiene & Tropical Medicine is one.

Please choose which qualification you would like to apply for. The link will take you directly to the University of London application portal.

• MSc Clinical Trials Gain the MSc Clinical Trials by completing 10 modules plus a final integrating report.  
• PGDip Clinical Trials Gain a Postgraduate Diploma in Clinical Trials by completing 8 modules.  
• PGCert Clinical Trials Gain a Postgraduate Diploma in Clinical Trials by completing 4 modules.  
• Individual modules Study a module as a short course.

1. Submit your application to University of London. Please read the Guidance Notes for Applications (pdf)  before you complete your application.

2. Submit your documentary evidence. This can be done online when submitting your application or at a later stage. You will be required to submit personal identification, educational certificates, transcripts, English language proficiency evidence, references and CV (see  Guidance Notes for Applications (pdf)  for further details).

3. University of London will notify you of whether or not you have been accepted. This usually happens within five working days. You will be sent a student reference number by email in case you need to contact University of London about your application.

4. If you are made an offer, you will receive an email with instructions for completing your online registration (usually from May/June). You will have until the registration deadline to accept your offer and pay your initial fees.

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Highlights on Future Treatments of IPF: Clues and Pitfalls

Alessandro libra.

1 Department of Clinical and Experimental Medicine, Regional Referral Center for Rare Lung Disease, Policlinico “G. Rodolico-San Marco”, University of Catania, 95123 Catania, CT, Italy; ti.kooltuo@arbilordnassela (A.L.); moc.liamg@92accaicse (E.S.); [email protected] (G.M.); [email protected] (L.S.)

Enrico Sciacca

Giuseppe muscato, gianluca sambataro.

2 Artroreuma s.r.l., Rheumatology Outpatient Clinic, 95030 Mascalucia, CT, Italy; moc.liamg@oratabmasrottod

Lucia Spicuzza

Carlo vancheri, associated data.

Not applicable.

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by irreversible scarring of lung tissue, leading to death. Despite recent advancements in understanding its pathophysiology, IPF remains elusive, and therapeutic options are limited and non-curative. This review aims to synthesize the latest research developments, focusing on the molecular mechanisms driving the disease and on the related emerging treatments. Unfortunately, several phase 2 studies showing promising preliminary results did not meet the primary endpoints in the subsequent phase 3, underlying the complexity of the disease and the need for new integrated endpoints. IPF remains a challenging condition with a complex interplay of genetic, epigenetic, and pathophysiological factors. Ongoing research into the molecular keystones of IPF is critical for the development of targeted therapies that could potentially stop the progression of the disease. Future directions include personalized medicine approaches, artificial intelligence integration, growth in genetic insights, and novel drug targets.

1. Introduction

Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease (ILD) characterized by irreversible scarring of lung tissue and destruction of lung architecture, exhibiting radiological and histological characteristics consistent with usual interstitial pneumonia [ 1 ]. IPF represents, as a form of idiopathic interstitial pneumonia, a subset of fibrotic lung disorders that lack a discernible cause, making its etiology elusive and understanding of its pathogenesis challenging.

The pathologic hallmark of IPF is the aberrant deposition of collagen and other extracellular matrix components within lung parenchyma, leading to impaired gas exchange and altered lung function [ 2 ]. This condition predominantly affects individuals in their sixth decade of life, presenting an insidious onset, progressive nature, and limited therapeutic options. Patients with IPF report symptoms like dyspnea, dry cough, and fatigue [ 1 ]. However, the non-specific nature of these symptoms poses significant challenges in early diagnosis; consequently, IPF is frequently diagnosed at advanced stages, limiting the effectiveness of therapeutic interventions [ 3 ]. Unraveling the pathogenesis of IPF has been a subject of intensive research, revealing complex interactions among genetic predisposition, environmental factors, and dysregulated host responses. Alveolar epithelial cell (AEC) injury, abnormal wound healing responses, and dysregulation of fibroblast activation are key cellular events implicated in the initiation and perpetuation of the fibrotic cascade [ 2 , 4 ]. A deeper understanding of the molecular and cellular mechanisms involved in IPF is essential for the development of targeted therapies that can stop or reverse the progression of this devastating disease. Despite advancements in the understanding of IPF pathobiology, therapeutic options remain limited. Antifibrotic agents, such as pirfenidone and nintedanib, have emerged as the mainstay of treatment, aiming to slow disease progression. However, these drugs are not curative, and the need for novel therapeutic modalities that address the underlying pathogenic processes is evident. The complex and multifaceted nature of IPF needs more research efforts to fully elucidate its underlying mechanisms. The absence of a definitive cure has encouraged investigations in the field of IPF. However, a significant number of trials, particularly those in phase III, have failed to achieve the primary endpoint [ 5 ].

This review aims to contribute to the collective knowledge that will pave the way for innovative approaches to treatment and to provide a deeper understanding of the latest developments in the pathogenesis of IPF, highlighting recent progress in pharmaceutical interventions for IPF.

2. Genetics, Risk Factors, and Epigenetic Changes in the Pathogenesis of IPF

Genetic factors play a fundamental role in the development of IPF. Genetic variants associated with IPF are classified into two categories: single nucleotide polymorphisms (SNPs) found in the general population with an allele frequency greater than 1% and rare variants with an allele frequency lower than 1%, usually not present in the general population [ 6 ]. The development of next-generation sequencing (NGS) technologies has allowed a deeper exploration of the contribution of genomic variants to IPF development, focusing the attention on those variants involving two different biological pathways, namely telomere maintenance and surfactant metabolism [ 7 ]. Telomeres are specialized structures at the ends of chromosomes with the function of protecting genome integrity and preventing end-to-end chromosomal degradation and fusion [ 8 ]. During DNA replication, the extreme ends of chromosomes cannot be copied, leading to progressive telomere shortening with each cell division. Telomerases are enzymes that add repeated sequences to the ends of chromosomes to compensate for this telomere shortening. However, these enzymes have limited activity and gradually lose their function, ultimately resulting in cellular senescence and apoptosis [ 9 ]. Telomerases involve a catalytic subunit, telomerase reverse transcriptase (TERT), and the RNA component of telomerase (TERC). Genetic defects altering the activity of TERT and TERC were the first described and the most common in IPF patients [ 10 , 11 ]. With the development of NGS technology, numerous genetic variants contributing to the pathogenesis of IPF have been identified, showing that patients with mutations in telomere-related genes have shortened telomeres that may lead to an early onset of the disease [ 7 ]. Pulmonary surfactant is a mixture of lipids and proteins produced by type II AEC. In addition to playing a role in host defense and modulating the immune response, its primary function is to reduce the surface tension of alveoli, preventing their collapse. Mutations in these genes predispose individuals to a wide range of fibrotic lung diseases [ 12 , 13 , 14 , 15 ]. The genetic variant most strongly associated with IPF susceptibility is a SNP located in the promoter region of the MUC5B gene, identified as rs35705950 [ 16 , 17 ]. MUC5B encodes mucin 5B, a component of the mucus on the surface of the bronchial mucosa, and is associated with the failure of alveolar repair, regeneration mechanisms, and mucociliary dysfunction [ 18 , 19 ]. Genetic variants of MUC5B cause its overexpression in bronchoalveolar epithelium and represent one of the main genetic risk factors for both familial and sporadic IPF, although the precise mechanism involved in disease induction is not yet clear [ 20 , 21 ]. Cigarette smoke is one of the primary risk factors for chronic respiratory diseases, including IPF [ 22 ]. It can cause damage to all types of lung cells, but it particularly harms AEC, triggering the fibrogenic process [ 23 ]. Cigarette smoke increases the risk of IPF, with smokers having a 60% higher risk [ 24 ]. In addition to cigarette smoke, particulate matter, fibers, and dust are major environmental risk factors contributing to the onset of IPF [ 25 ]. An increased incidence of the disease was observed in individuals exposed to inorganic dust, chemical fumes, and other pollutants [ 26 ]. These substances, following prolonged exposure, result in epithelial damage and oxidative stress, leading to senescence of AEC type II with consequent fibrosis [ 27 , 28 ]. These risk factors can induce epigenetic alterations, such as DNA methylation, histone modification, and non-coding RNA gene silencing, which play a key role in the development of pulmonary fibrosis [ 29 , 30 , 31 ]

3. Overview of Current Pathogenic Hypothesis

IPF is characterized by the excessive production and disorganized deposition of extracellular matrix (ECM) components, resulting in irreversible architectural distortion and loss of organ function [ 32 ]. One crucial player in the multifaceted pathogenesis of IPF is transforming growth factor (TGF)-β. Released in response to epithelial cell injury, TGF-β acts as a central pro-fibrotic growth factor, driving the progression of pulmonary fibrosis [ 33 ]. Its multifunctional nature stimulates the proliferation and differentiation of epithelial cells and fibroblasts, activates myofibroblasts to generate ECM, catalyzes epithelial-mesenchymal transition (EMT), expedites epithelial apoptosis and cell migration, and induces the production of connective tissue growth factor (CTGF) and other mediators [ 26 , 34 ]. Insulin-like growth factor (IGF) also contributes significantly to the progression of pulmonary fibrosis [ 35 , 36 ]. IGF-1 plays a role in mediating various biological functions, including fibroblast proliferation, migration, and differentiation. This enhances the ability of fibroblasts to synthesize fibronectin and collagen, ultimately leading to increased ECM deposition [ 37 , 38 ].

CTGF, as a cysteine-rich stromal cell protein, influences numerous biological processes, such as cell proliferation, differentiation, adhesion, and angiogenesis [ 39 ]. It acts as a primary mediator of TGF-β-induced pulmonary fibrosis, directing tissue regeneration and pathological fibrosis formation through ECM deposition, fibroblast proliferation, and matrix generation [ 40 , 41 ]. Matrix metalloproteinases (MMPs), including MMP-3, MMP-7, and MMP-8, actively contribute to pulmonary fibrosis by regulating EMT and influencing abnormal repair processes [ 42 , 43 ]. MMP-7, in particular, is elevated in both human IPF and mouse fibrosis models, and higher levels are associated with an increased risk of mortality and disease progression [ 44 ]. Exosomes, phospholipid bilayer membranous vesicles, also play a significant role in the pathogenesis of IPF [ 45 ]. Continuously secreted by various cell types, they transport biologically active substances, such as proteins, lipids, and genetic material. In the lungs, alveolar and bronchial epithelial cells primarily generate exosomes, which activate fibroblasts, stimulate their differentiation into myofibroblasts, and catalyze excessive ECM component deposition [ 46 ]. Aging further contributes to IPF by depleting type 2 AEC, impairing the alveoli’s ability to repair injury. IPF lung tissue exhibits several characteristics of aging lungs, including cellular senescence, telomere shortening, mitochondrial and lysosomal/autophagy dysfunction, and epigenetic changes [ 14 , 15 ].

Tumor necrosis factor-alpha (TNF-α), a pro-inflammatory cytokine, significantly contributes to the recruitment and activation of immune cells, exacerbating tissue damage and fibrosis. TNF-α directly stimulates pulmonary fibroblasts, increasing the production of extracellular matrix and fibrogenic growth factors, creating a pro-fibrotic environment [ 47 ]. Interleukins (IL), particularly IL-1β, IL-6, and IL-13, promote fibroblast proliferation and collagen deposition, enhancing extracellular matrix remodeling and scarring of lung tissue [ 48 ].

In summary, the intricate pathogenesis of IPF ( Figure 1 ) involves a dynamic interplay of factors, including TGF-β, IGF, CTGF, MMPs, exosomes, TNF-α, and interleukins, all contributing to the excessive production and deposition of ECM components, ultimately resulting in irreversible architectural distortion and loss of organ function. Understanding these mechanisms provides potential avenues for therapeutic interventions in IPF.

Overview of the most significant pathogenic pathways involved in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and molecules currently under clinical investigation and their mechanisms of action within the pathways implicated in IPF pathogenesis. Legend: AEC: alveolar epithelial cells; EMT: epithelial-mesenchymal transition; PDE-4B: phosphodiesterase-4B; ECM: extracellular matrix; MAPK/ERK: mitogen-activated protein kinase/extracellular signal-regulated kinase; LPA1: lysophosphatidic acid receptor 1; C/EBPβ: CCAAT/enhancer binding protein beta; mAb: monoclonal antibody; Bcl-2: B-cell lymphoma 2; TGF-β: transforming growth factor beta; GF: growth factor; TNF-α: tumor necrosis factor alpha; IL: interleukin; OSMR: oncostatin M receptor; CSF-1R: colony stimulating factor 1 receptor; PD-L1: programmed death—ligand 1; Smad3: SMAD family member 3; MSCs: mesenchymal stem cells; STAT3: signal transducer and activator of transcription 3; JAK1/2: Janus kinase 1/2.

4. Future Therapeutic Perspectives Based on Current Pathogenic Knowledge

Current approved anti-fibrotic drugs, pirfenidone and nintedanib, target multiple known aspects of IPF. Pirfenidone reduces TGF-β expression and activation, mitigating fibroblast activation and collagen synthesis [ 49 ]. Pirfenidone also exhibits anti-inflammatory properties by suppressing pro-inflammatory cytokines and chemokines, reducing lung inflammation [ 50 ].

Nintedanib, a tyrosine kinase inhibitor, targets receptors involved in fibrosis such as vascular endothelial growth factor receptor (VEGFR), fibroblast growth factor receptor (FGFR), and platelet-derived growth factor receptor (PDGFR) [ 51 , 52 ].

Several molecules are under investigation in various clinical trial in different phases. The main clinical trials related to ongoing studies for IPF therapy are summarized in Table 1 .

An overview of clinical trials of in IPF.

Legend: PDE-4B: phosphodiesterase-4B inhibitor; ECM: extracellular matrix; LPA1: lysophosphatidic acid; LPAR1: lysophosphatidic acid receptor 1; C/EBPβ: CCAAT/enhancer-binding protein beta; ENO1: alpha-enolase; mAb: monoclonal antibody; TGF-β1: transforming growth factor-β 1; OSMR: oncostatin M receptor; CSF-1R: colony-stimulating factor-1 receptor; PD-L1: programmed death—ligand 1; STAT3: signal transducer and activator of transcription 3; JAK1/2: Janus kinase 1/2 inhibitor.

4.1. The Role of Fibroblasts

In healthy lung tissue, fibroblasts play a crucial role in regulating wound healing and tissue repair. They are primarily responsible for synthesizing and remodeling the ECM, thus ensuring tissue homeostasis [ 32 ]. In the context of IPF, recurrent injurious triggers, along with a compromised function of the alveolar epithelium, change the cytokine balance within lung tissue. The alteration of the tissue microenvironment is characterized by elevated levels of profibrotic molecules such as platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and TGF-β [ 53 ]. This promotes the transformation of fibroblasts into myofibroblasts (FMT) and the inhibition of the subsequent programmed cell death of these cells [ 54 ]. This process is marked by the proliferation of resident mesenchymal cells, the attraction of circulating fibrocytes, and the stimulation of EMT [ 55 ]. Emerging evidence suggests that epithelial cells undergoing EMT may also contribute to the pool of activated myofibroblasts in IPF [ 53 ]. Activated fibroblasts and myofibroblasts in IPF are prolific producers of ECM components, particularly collagen. This uncontrolled deposition of ECM results in lung stiffening and impaired gas exchange, contributing to the characteristic decline in lung function seen in IPF patients [ 56 ].

Tyrosine kinase and its receptor are also involved in regulating cell growth and fibroblast behavior. In 2014, FDA approved nintedanib, a tyrosine kinase receptor inhibitor, for the treatment of IPF [ 57 ]. Anlotinib represents a novel class of small-molecule, multi-target tyrosine kinase inhibitors. Its mechanism of action is based on the suppression of the activity of VEGFR, PDGFR, FGFR, and various other kinases. It received regulatory approval in China in 2018 and has gained significant utilization in anti-angiogenesis therapy for lung cancer patients in recent years [ 58 ]. In addition, preclinical studies have shown that anlotinib can inhibit the proliferation of AEC-induced EMT and pulmonary fibroblasts by inhibiting the TGFβ-1 signaling pathway. In addition, anlotinib inhibits pulmonary fibrosis by down-regulating the poly(rC)-binding protein 3 (PCBP3) expression, reducing 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) translation, and inhibiting glycolysis of fibroblasts [ 59 , 60 ]. A phase 2–3 trial (NCT05828953) is recruiting patients with IPF/progressive fibrosing interstitial lung diseases (PF-ILDs) diagnoses to evaluate the effectiveness of anlotinib hydrochloride capsules in reducing forced vital capacity (FVC) decline.

Treprostinil is a full prostacyclin receptor (IP) agonist that has high affinity for prostaglandin E receptor 2 (EP2) and the prostaglandin D receptor 1 (DP1). Binding to and activating EP2, IP, DP1, and peroxisome proliferator-activated receptor β (PPARβ) receptors lead to a range of antifibrotic effects [ 61 ]. When EP2, IP, and DP1 receptors are activated, they cause vasodilation and help reduce fibroblast activity, proliferation, collagen deposition, and inflammation. Specifically, EP2 activation inhibits the transformation of fibroblasts into myofibroblasts and reduces collagen overproduction [ 62 , 63 ], while DP1 activation decreases the recruitment of inflammatory cells and the synthesis of the extracellular matrix [ 64 ]. Additionally, activating the PPARβ receptor suppresses fibroblast proliferation [ 65 ]. Together, these actions promote vasodilation, minimize vascular remodeling, and reduce fibrosis. The INCREASE trial was a randomized, placebo-controlled, phase 3 study that assessed the effects of inhaled treprostinil in patients with ILD and associated pulmonary hypertension. The trial found that treprostinil significantly improved exercise capacity from baseline to week 16, as measured by the 6-min walk test, compared to placebo. Additionally, the study showed improvements in forced vital capacity (FVC) and reduced exacerbations of the underlying lung disease [ 66 ]. Beyond achieving the primary endpoint (6-min walk distance) and secondary endpoints, a post hoc analysis revealed significant improvements in FVC for subjects with PH-ILD treated with inhaled treprostinil [ 67 ]. These results, along with preclinical evidence of treprostinil’s antifibrotic activity, suggest that inhaled treprostinil may be a treatment option for patients with IPF. Currently, the TETON program includes two phase 3 randomized, double-blind, placebo-controlled studies (NCT04708782, NCT05255991) that are investigating the efficacy and safety of inhaled treprostinil in idiopathic pulmonary fibrosis [ 68 ].

Phosphodiesterases (PDEs) are the main superfamily of enzymes responsible for degrading the secondary messengers cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Inhibiting these enzymes results in a decrease in prostaglandin E2 levels, which plays a crucial role in fibroblast function. [ 69 ] BI 1015550, a phosphodiesterase-4B (PDE-4B) inhibitor, has shown potential in preclinical models to inhibit TGFβ1-induced myofibroblast transformation and extracellular matrix deposition [ 70 ]. A phase 2 double-blind, placebo-controlled, parallel-design trial showed that patients treated with BI 1015550 had a smaller median decline, or a slight improvement, in FVC at 12 weeks compared to the placebo group (median difference of 62–84 mL) [ 71 ]. The FIBRONEER phase 3 program is currently recruiting globally to assess BI 1015550 in IPF (NCT05321069).

Caveolin-1 (Cav-1) is another crucial regulator of TGF-β signaling. TGF-β receptors internalized through Cav-1 undergo rapid degradation, reducing TGF-β signaling. Cav-1 deficiency results in increased collagen gene expression in human lung fibroblasts. Restoration of Cav-1 function using a cell-permeable peptide carrier for a bioactive Cav-1 fragment has shown to reduce fibrosis, indicating Cav-1 as a potential therapeutic target for pulmonary fibrosis [ 72 ]. Cav-1 influences the mitogen-activated protein kinases/ extracellular signal-regulated kinases (MAPK/ERK) signaling pathway in lung fibroblasts. A decrease in Cav-1 expression leads to increased MAPK/ERK activation and collagen expression. This shows that Cav-1 plays a role in a branched signaling pathway that regulates collagen expression in lung fibroblasts, damaged during fibrotic process [ 72 ]. A marked reduction in Cav-1 expression is observed in lung tissues and pulmonary fibroblasts from IPF patients. Cav-1’s ability to suppress TGF-β1-induced ECM production through the regulation of the c-Jun N-terminal kinases (JNK) pathway has been highlighted [ 73 ]. Based on this evidence, the LTI-03 (NCT05954988) study will investigate the caveolin-1-scaffolding-protein-derived Peptide, recruiting IPF patients for a phase 1 clinical trial.

Lysophosphatidic acid (LPA) also plays a role in the pathogenesis of IPF, particularly through its interactions with fibroblasts. Recent research has revealed significant insights into how LPA and its related pathways contribute to IPF. LPA signaling occurs through receptors found in various cells, including AEC, vascular endothelial cells, and fibroblasts. LPA receptor inhibitors and metabolic enzymes involved in LPA formation may represent potential targets for treating IPF [ 74 ]. In this context, the LPA1 receptor has emerged as a promising therapeutic target. A novel LPA1 antagonist, BMS-986278, has shown efficacy in preclinical studies by inhibiting LPA-stimulated responses in primary human lung fibroblasts and showing antifibrotic activity in animal models. This finding suggests that targeting LPA1 could slow the progression of IPF [ 75 ]. In 2023, a phase 3 study (NCT06003426) started recruiting participants with IPF to test BMS-986278. Phase 2 results were encouraging, showing a significantly slowed rate of FVC decline [ 76 ]. Following the lead of BMS-986278, a LPAR1 antagonist (NCT05032066) coded as HZN-825 will be investigated for its potential in treating IPF and systemic sclerosis (SSc).

The enzyme autotaxin, which generates most extracellular LPA, is also implicated in the development of lung fibrosis. Elevated autotaxin expression was found in the lungs of IPF patients, and the inhibition of this enzyme limits the development of pulmonary fibrosis in animal models [ 77 ]. This recent finding places autotaxin as an interesting new target for IPF and other fibrotic diseases [ 78 ]. Unfortunately, the ISABELA 1–2 trials (NCT03711162-NCT03733444) that tested ziritaxestat, an autotaxin inhibitor, in patients with IPF did not improve clinical outcomes compared with placebo [ 79 ].

The chronic activation and prolonged presence of myofibroblasts within tissues are related to the progression of fibrosis [ 80 ]. CCAAT/enhancer-binding protein beta (C/EBPβ) is emerging as a critical factor in the pathogenesis of IPF, particularly through its interactions with fibroblasts and effect on myofibroblast differentiation. Studies, such as the one conducted by Ding et al., reveal that C/EBPβ acetylation is significantly elevated in IPF, especially within fibroblast foci. This acetylation correlates with an increase in α-smooth muscle actin (α-SMA) and collagen-I, markers indicative of pulmonary fibrosis. This finding underscores the involvement of acetylated C/EBPβ in the development of pulmonary fibrosis and suggests a potential target for therapeutic intervention [ 80 , 81 ]. XFB19 (NCT05361733) is a first-in-class synthetic tetra-peptide (Acetyl-Lys-D-Ala-D-Val-Asp-NH2) that inhibits the activation of the human C/EBPβ, thus mediating the activation of lung myofibroblasts.

MMP7, also known as matrilysin, is a member of the matrix metalloproteinase family of enzymes that are involved in the degradation and remodeling of ECM components in the lung tissue, expressed by lung epithelial cells, mononuclear phagocytes, and fibrocytes [ 82 ]. Moreover, increased levels of MMP7 were found in sputum and bronchoalveolar lavage (BAL) of patients with IPF, suggesting a plausible role in fibrogenesis and a possible role as a biomarker [ 83 , 84 ]. A clinical trial is going to test ARO-MMP7, an RNA interference (RNAi), as a therapeutic candidate [ 85 ] that targets MMP7 expression, aiming at, as the primary outcome, the changes in MMP7 concentration in BAL (NCT05537025).

4.2. The Role of Macrophages

It is known that macrophages contribute to the maintenance of tissue homeostasis, immune regulation, and pathogen clearance [ 86 ]. Within the lungs, there are different types of macrophages, such as alveolar macrophages (AMs) and interstitial macrophages (IMs), each with different characteristics, responsible for specific responses to different signals [ 87 ]. Macrophages are fundamental for the regulation of lung immunity, acting as a major component of the innate immune system and providing a link with adaptive immunity. They play a significant role in responding to toxic exposures and environmental challenges [ 88 ]. Their heterogeneity and plasticity enable them to efficiently respond to various cytokines and microbial signals [ 89 ]. Their motility allows them to migrate within lung tissues, adapting their function to their environment and playing roles ranging from phagocytic scavengers to microbicidal effectors [ 90 ]. Apoptosis resistance in monocyte-derived macrophages (MDMs) is a notable feature of IPF. MDMs isolated from the BAL of patients with IPF, exhibit increased mitochondrial biogenesis partly due to heightened expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), a coactivator regulating mitochondrial dynamics. This contributes to apoptosis resistance in MDMs [ 91 ]. Elevation of mitochondrial Bcl-2 is linked instead to interactions with carnitine palmitoyltransferase 1a (Cpt1a), which binds to Bcl-2’s BH3 domain, anchoring it in the mitochondria to reduce apoptosis. Consequently, modulating the interaction between Cpt1a and Bcl-2 in macrophages could influence fibrotic remodeling and apoptosis resistance [ 91 ]. Based on this preclinical evidence, a new drug, venetoclax, a new Bcl-2 inhibitor and BH3 domain blocker, has been shown to induce apoptosis of MDMs and reverse established fibrosis [ 92 , 93 ]. The NCT05976217 study is recruiting to test venetoclax in an early phase 1 clinical trial. ENO1, also known as alpha-enolase, is a multifunctional glycolytic enzyme involved in various physiological processes. It plays a crucial role in glycolysis, the metabolic pathway that converts glucose into pyruvate, generating ATP and NADH in the process. ENO1 is also involved in other non-glycolytic functions, such as cell signaling, transcriptional regulation, and cell migration [ 94 ]. In addition, ENO1 interacts with human plasminogen, suggesting its involvement in the regulation of fibrinolysis and ECM remodeling [ 95 ]. HuL001 is an anti-ENO1 monoclonal antibody that will be investigated in a phase 1 clinical trial (NCT04540770).

4.3. The Role of TGF-β

Repeated, chronic damage to AEC causes an elevated secretion of profibrotic cytokines and chemokines [ 96 ]. The increased release of fibrogenic signaling molecules, like TGF-β, promote recruitment, propagation, and transformation of fibroblasts into myofibroblasts. TGF-β increases collagen synthesis, exerting its influence on the primary collagen-producing cells [ 27 , 28 ]. Additionally, TGF-β stimulates production of other fibrogenic molecules, such as CTGF, FGF, IGF, and PDGF. TGF-β is not only a potent stimulator of ECM production; it is also known as the most potent attractant for immune cells, encompassing monocytes and macrophages [ 97 ]. Pirfenidone, one of two antifibrotic drugs approved for treatment of IPF, plays a role as an antifibrotic agent exhibiting proficient inhibition of fibronectin and α-SMA expression, both pivotal factors in the EMT transition induced by TGF-β [ 98 , 99 , 100 ]. Sufenidone (NCT06125327), deupirfenidone (NCT05321420), and yifenidone (NCT05060822) are three molecules with a chemical structural similar to pirfenidone. While sufenidone seems to have a protective effect on pulmonary fibrosis in mouse models [ 101 ], deupirfenidone and yifenidone are derived forms of pirfenidone designed to attenuate the rate of drug metabolism, resulting in a differentiated pharmacokinetic profile that maintains the efficacy of pirfenidone with a potential improvement of tolerability [ 102 , 103 ].

SRN-001 (NCT05984992) represents an innovative small interfering RNA (siRNA) under development for the treatment of fibrosis (phase 1). Amphiregulin (AREG), a growth factor intricately involved in fibroblast proliferation and differentiation into myofibroblasts, stands as a pivotal player in the characteristic fibrosis observed in lung tissues [ 104 ]. AREG emerges as a downstream gene excessively expressed by TGF-β during fibrosis, thereby instigating FMT [ 105 ]. Through the mechanism of RNA interference (RNAi), SRN-001 is designed to attenuate the production of amphiregulin, aiming to modulate the fibrotic processes.

Integrins constitute an extensive group of transmembrane glycoprotein receptors originally recognized for their roles in cell adhesion and maintenance of tissue integrity. Among these, integrin αVβ6 plays a crucial role in the activation of latent TGF-β, exhibiting a mechanism that enables control of its activity [ 106 ]. Bexotegrast (NCT06097260), inhibiting integrins αVβ1 and αVβ6, which in turn blocks the activation of TGF-β [ 107 , 108 ], is currently in a phase 2 trial aimed to evaluate efficacy and safety.

Artesunate is a semi-synthetic artemisinin, widely used in clinical antimalarial treatment. Several studies have demonstrated the role of artesunate in downregulating the expression of profibrotic mediators, such as TGF-β1, in rats with bleomycin-induced pulmonary fibrosis [ 109 , 110 ]. According to these concepts, a phase 1 study evaluating the safety and tolerability of artesunate with escalating doses is currently ongoing (NCT05988463).

4.4. New Therapeutic Strategies: Monoclonal Antibody

Current medical practices have undergone a transformative shift towards tailored treatments addressed to individualized disease characteristics. Monoclonal antibodies (mAbs) serve as an illustration of personalized therapeutics, made possible through advances in our understanding of immunology, molecular biology, and biochemistry.

CTGF’s role in regulating myofibroblast activation, ECM deposition, and fibrotic remodeling through TGF-β downstream signaling is considered a key factor of IPF pathogenesis [ 111 , 112 , 113 ]. The PRAISE phase 2 trial investigated the effects of pamrevlumab, a recombinant human antibody against CTGF, on the decline in the percentage of predicted FVC at week 48. Pamrevlumab reduced the decline in the percentage of predicted FVC, and positive treatment outcomes were evidenced, such as the improvement of some radiological findings (quantitative lung fibrosis score at HRCT) and symptoms. The promising results from the phase 2 trial led to the initiation of a phase 3 program consisting of two identical trials (ZEPHYRUS I and II), (NCT03955146 and NCT04419558). Unfortunately, this program faced premature termination in June 2023, as the ZEPHYRUS I study did not meet the primary endpoint. Vixarelimab is another human monoclonal antibody that targets oncostatin M receptor beta (OSMRβ), which mediates signaling of interleukin-31 (IL-31) and oncostatin M (OSM). The rationale for a clinical trial with this antibody is based on the evidence that loss of IL-31 signaling attenuates bleomycin-induced pulmonary fibrosis, while elevated expression levels of OSM have been noted in various inflammatory conditions, including those accompanied by fibrotic complications [ 114 , 115 ]. Although its involvement in fibrosis is currently under investigation, existing evidence indicates that this cytokine possesses the capacity to stimulate inflammation, induce vascular injury, and activate fibroblasts [ 115 ]. Actually, vixarelimab is in a phase 2 clinical trial, aimed to evaluate changes in FVC from baseline to week 52 (NCT05785624). Axatilimab is an experimental monoclonal antibody designed to target the colony-stimulating factor-1 receptor (CSF-1R), a cell surface protein believed to control survival and functionality of monocytes and macrophages. Inhibiting signaling through the CSF-1 receptor is effective in reducing the number of disease-contributing macrophages and their monocyte precursors [ 116 ]. This reduction may play an essential role in mitigating the fibrotic disease processes associated with IPF. The ongoing phase 2 clinical trial is aiming to evaluate the efficacy and safety of axatilimab in patients with IPF (NCT06132256). EMT is an important pathogenic event in IPF, a phenomenon also observed in lung cancer, in which tumor cells express programmed death-ligand one (PD-L1) [ 117 ]. PD-L1 mediates lung EMT through Smad3 and β-catenin signaling pathways, contributing to fibrosis [ 118 , 119 ]. Based on this evidence, it is reasonable to suppose that immune checkpoint inhibitors such as atezolizumab may halt the progression of IPF, so a phase 1 clinical trial has already started to evaluate the safety and preliminary efficacy of atezolizumab (NCT05515627).

4.5. New Therapeutic Strategies: Stem Cells Therapy

In recent years, the use of embryonic stem cells for lung tissue regeneration has captured the attention of the scientific community. Stem cells exhibit notable anti-inflammatory and antifibrotic properties, positioning them as a potential therapy for fibrotic diseases, including IPF [ 120 , 121 ]. Several phase 1 clinical trials on stem cell therapy for IPF are currently ongoing, with the aim to assess the safety and feasibility of stem cell therapy (NCT05016817, NCT04262167, NCT01385644).

Mesenchymal stem cells (MSCs) are pluripotent cells with anti-inflammatory, immunosuppressive, and angiogenic functions, able to reduce extracellular matrix formation and collagen deposition. MSCs decrease the levels of TGF-β1 and TNF-α by producing prostaglandin E2 (PGE2) and hepatocyte growth factor [ 122 ]. Lung spheroid cells (LSC) comprise stem and support lung cells that can be cultured starting from lung tissue biopsies [ 123 ]. A study revealed that LSC treatment can attenuate and resolve bleomycin-induced fibrosis by reconstructing the normal alveolar structure, reducing collagen accumulation and myofibroblast proliferation [ 124 ]. When administered intravenously in a murine model of pulmonary fibrosis, lung spheroid cells demonstrated potent regenerative properties [ 125 ]. Some studies have shown encouraging results, with a significant improvement in FVC compared to the placebo group in patients receiving stem cell therapy [ 126 , 127 , 128 ]. Therefore, the use of stem cells in treating pulmonary fibrosis can be considered a promising future therapeutic strategy.

4.6. New Therapeutic Strategies: Tyrosine Kinase Inhibitors

Protein kinases have been associated with the fibrogenic process mediated by growth factors like TGF-β [ 129 ]. Activation of tyrosine kinases, particularly receptor tyrosine kinases (RTKs), results in the phosphorylation of tyrosine residues on target proteins, initiating cascades of intracellular signaling events. Dysregulation of tyrosine kinase activity was observed in various cell types within the lungs of IPF patients, including fibroblasts, epithelial cells, and inflammatory cells. This may contribute to the initiation and perpetuation of pro-fibrotic processes such as excessive ECM deposition and differentiation of fibroblasts into myofibroblasts. Several growth factor receptors and cytokine receptors, acting either as tyrosine kinases or able to activate tyrosine kinases upon ligand binding, are involved in the pathogenesis of IPF. Notably, receptors for PDGF, FGF, and epidermal growth factor (EGF) activate tyrosine kinases and are associated with fibrotic responses [ 130 , 131 ]. In addition to RTKs, non-receptor tyrosine kinases, including members of the Src family, also contribute to the pathogenesis of lung fibrosis [ 132 ]. These kinases are activated by various extracellular signals and mediate downstream effects that promote fibrosis, including cell proliferation, migration, and ECM remodeling. Tyrosine kinase inhibitors are currently utilized in the treatment of IPF for the selective inhibition of fibroblasts [ 130 ]. Nintedanib is an intracellular antagonist that selectively inhibits a range of tyrosine kinases, including the receptors for VEGF, FGF and PDGF [ 133 ]. Currently, it stands as one of the two approved antifibrotic treatments for IPF [ 1 , 51 , 134 ]. Understanding the specific tyrosine kinase pathways involved in IPF may provide additional potential targets for therapeutic intervention. Inhibitors targeting these kinases are currently explored as potential treatments to modulate aberrant signaling cascades and mitigate the fibrotic processes associated with IPF [ 57 ]. Saracatinib is a selective Src kinase inhibitor originally developed for oncological indications. Considering that Src-dependent processes also regulate myofibroblast differentiation and fibrogenic gene expression, a phase 1b/2a clinical trial has started to evaluate the use of saracatinib in the treatment of IPF (NCT04598919) [ 135 , 136 ].

The Janus kinase/signal transducer and activator of transcription (JAK/STAT) molecular pathway becomes activated in response to the interplay of a diverse array of profibrotic/pro-inflammatory cytokines and growth factors that are overexpressed in IPF, including PDGF, TGF-β1, and FGF [ 136 , 137 ]. These factors trigger JAK/STAT activation through both the canonical and non-canonical pathways, highlighting the relevant involvement of JAK/STAT in the fibrogenic process. Based on these findings, several clinical trials have addressed the evaluation of safety and efficacy of different drugs sharing the ability to block the JAK/STAT pathway (NCT05671835, NCT04312594).

5. Discussion

In recent years, significant progress has been made in the understanding of the pathobiology of IPF; however, these advancements are not fully satisfactory, and the approved drugs are still not curative. They may slow the decline of FVC, increasing survival, but are not able to block or reverse lung damage [ 138 ]. The primary goals of IPF patient management remain symptom alleviation, improvement in quality of life, and preservation of lung function over time. Even so, the identification of new potential therapeutic targets has been challenging, and the translation of these advances into drug development has been largely unproductive. It is important at this point to explore the possible pitfalls that determined the failure of several clinical trials, even in advanced phases. Most preclinical studies are performed on animals with experimentally induced fibrosis, keeping in mind that pharmacologically induced animal models of pulmonary fibrosis do not precisely reproduce the histological and pathophysiological patterns of IPF. Therefore, there is a need to identify animal models that more closely resemble IPF. Some clinical trials were prematurely terminated due to failure to reach the primary endpoint [ 5 ]. A possible explanation for this phenomenon may be the relative short observation period of 24 weeks for a disease characterized by an unpredictable course with phases of functional stability alternating with more rapid clinical worsening. This may also increase, particularly in phase 2 studies, the risk of excluding potentially promising molecules due to the incorrect selection of primary endpoints.

As regards endpoints of clinical trials, several studies have unequivocally demonstrated how FVC represents the main mortality predictor in IPF [ 139 , 140 , 141 ]. The role of FVC is further confirmed by its importance for the definition of PF-ILD [ 142 ]. On the other hand, a recent new point of view is considering replacing FVC as the primary endpoint with composite endpoints that include “feels, functions, survives” measures, with FVC as one of the components [ 143 ]. In recent years, several trials have initially given importance to the 6-min walking test (e.g., NCT04552899, NCT04396756) that was gradually abandoned due to the variability of the test within trials [ 144 ]. In addition, IPF still suffers due to late diagnoses often made in patients with very low DLCO values, between 25 and 30% [ 145 ]. Consequently, the trend of the latest clinical trials is to “lower the bar” to make patient participation more accessible. In considering the quest for the most accurate endpoint, it becomes pertinent to assess the real potential of composite endpoints. These endpoints, allowing the inclusion of multiple significant domains within a single predetermined endpoint, confer numerous advantages [ 146 ]. They facilitate a more comprehensive portrayal of a drug’s effects, predicting a range of events such as categorical alterations in FVC or the 6-min walking test distance, occurrences of respiratory hospitalization, changes in functional classification, transplant, or mortality.

It is known that not all IPF patients have the same course of the disease, with some being relatively “long survivors” and others with a more rapid progression of the disease possibly marked by exacerbations and in some cases affected by the presence of relevant comorbidities [ 147 ]. This makes IPF patients an extremely heterogeneous group, where each patient may have an individual response to the explored new drug. This individual response may be associated with different pathophysiological mechanisms, including the activation of specific pathways. The use of composite endpoints among patients enrolled in clinical trials may reduce this heterogeneity avoiding the fragmentation of these patients in small subgroups. As the understanding of the molecular mechanisms underlying IPF improves, it may be possible to devise personalized treatment strategies targeting specific pathways or genetic factors in individual patients.

Given the recognized role of TGF-beta in the pathogenesis of IPF, it is plausible that two drugs with complementary mechanisms may be more effective. A pharmacological treatment involving the use of multiple drugs should be taken into consideration. The INJOURNEY study evaluated the add-on therapy between pirfenidone and nintedanib with promising results in terms of safety and some preliminary insight into efficacy [ 148 ]. Unfortunately, this study was not followed by a larger trial specifically powered for the evaluation of efficacy. More recently, Bonella et al. highlighted that most experimental new drugs are evaluated as adjunctive therapy to the already approved antifibrotic therapies. Considering the intriguing possibility of targeting multiple coactivated profibrotic pathways, the optimal drug partners are those with complementary, alternative, or synergistic mechanisms of action compared to the standard of care [ 149 ]. In oncology, tailored and combined treatments represent a therapeutic keystone, always based on a careful evaluation of the individual patient characteristics, including a molecular and histopathological assessment. Over time, IPF was compared with cancer [ 97 , 150 , 151 , 152 ]. Both IPF and lung cancer are marked by epigenetic modifications, such as DNA methylation and histone modifications, that may alter gene expression without changing the DNA sequence. These epigenetic changes affect genes associated with cell cycle control, apoptosis, and ECM remodeling, processes known to be associated with both fibrosis and cancer [ 153 , 154 ]. Both diseases have limited treatment options and are associated with high mortality rates. However, the shared pathogenic pathways also present opportunities for novel therapeutic strategies [ 151 ]. Repositioning of drugs already used in oncology could be an interesting option for the treatment of IPF, taking advantage of the multiple shared pathogenic mechanisms between the two diseases. Nintedanib, originally used for the treatment of lung cancer, is the practical demonstration of this concept. In oncology, artificial intelligence (AI), has demonstrated effectiveness in exploring genotypes and phenotypes for early diagnosis, screening, and personalized treatment regimens based on genetic-oriented features [ 155 ]. In respiratory diseases, AI and machine learning is mainly used to evaluate lung cancer and pulmonary fibrosis CT scan images [ 156 ]. More recently, for the first time in respiratory medicine, a new molecule developed entirely from AI, targeting alfa-SMA protein, will be tested in a phase 3 clinical trial for IPF treatment (NCT05938920) [ 157 ]. This AI-designed molecule may represent a breakthrough, as it demonstrates the potential of AI in accelerating drug discovery processes by predicting the structure and function of novel molecules. These interesting results are likely indicating a new different approach for the identification of new molecules to treat IPF, suggesting that AI could play a pivotal role in the future of personalized medicine and targeted therapy development. Additionally, the integration of AI in respiratory medicine could lead to more personalized and effective treatment strategies, tailored to the specific genetic and molecular profiles of individual patients, thereby enhancing treatment outcomes and reducing adverse effects. These interesting results are likely indicating a new different approach for the identification of new molecules to treat IPF. Moreover, the role of genetic factors in the pathogenesis of IPF should not be underestimated. Over the years, significant progress was made in the potential application of gene therapy for the treatment of pulmonary fibrosis in vivo. Indeed, gene therapy may offer new and promising avenues to mitigate a broad range of processes involved in the development of fibrosis [ 158 ].

6. Conclusions and Future Perspective

Despite evident progress in understanding the pathophysiology of IPF and the increasing number of studies searching for new molecules capable of slowing or halting the progression of the disease, IPF still remains a clinical unsolved problem. The therapies currently available do not offer curative possibilities but aim to slow down the progression of the disease, still characterized by an unfavorable prognosis. This review provides insights into potential therapeutic targets and a more comprehensive evaluation of the entire pathogenetic process of IPF, which involves the activation of synchronous, multiple pathogenic pathways. A better understanding of the degree of activation of these pathways could lead to new approaches in the treatment of IPF, with targeted therapy adapted to the individual characteristics of each patient. Clinical trials must be based on robust, high-quality preclinical and clinical data, with precise and agreed-upon endpoints. There are many promising drugs in development, resulting from a continuous, yet insufficient investment in IPF research. Furthermore, our understanding of the pathogenesis of IPF remains limited, and it is imperative to direct our efforts towards in-depth insight into the mechanisms that underlie this complex disease and their impact on clinical phenotypes.

Funding Statement

This research received no external funding.

Author Contributions

Investigation, A.L. and E.S.; data curation, A.L. and E.S.; writing—original draft preparation, A.L. and E.S.; writing—review and editing, A.L., E.S., L.S. and C.V.; visualization, A.L., E.S., G.M. and G.S.; supervision, A.L., E.S. and C.V. All authors have read and agreed to the published version of the manuscript.

Institutional Review Board Statement

Informed consent statement, data availability statement, conflicts of interest.

C.V. is part of the F. Hoffmann-La Roche Ltd. and Boehringer Ingelheim Scientific board. He received consulting fees and/or speaker fees from AstraZeneca, Boehringer Ingelheim, C.F. Hoffmann-La Roche Ltd., and Menarini. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. G.S. reports personal fees from Boehringer Ingelheim outside the submitted work. A.L., E.S., G.M., and L.S. declare no conflicts of interest.

Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

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Imperial Clinical Trials Unit

A UKCRC registered, research-led, collaborative clinical trials unit

Our mission is to deliver excellence in the design, conduct and dissemination of clinical trials of all phases and through this to deliver major local, national and international health benefits for patients.‌

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Collaborate with ICTU

Investigators who are interested in collaborating with ICTU on your research idea - learn about our collaborations process and find out how to make an initial approach.

More about collaborating with ICTU

Clinical Data Systems

The Clinical Data Systems team works collaboratively with Imperial College Investigators, Researchers, Study Managers and Statisticians, and Study Teams to provide an electronic data capture system for your Clinical Research Study, in line with regulatory standards.

More about Clinical Data Systems

Imperial Clinical Trials Unit (ICTU) is a  UK Clinical Research Collaboration (UKCRC)  registered Clinical Trials Unit.

The Collaborations Section is currently being updated. 

If your request falls under one of the Therapeutic areas details for the relevant email can be found on the Therapeutic Area Contact Details  Page.

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Visit our dedicated website for commercial sponsors interested in working with ICTU.

Clinical Trials MSc

Distance learning programme

Clinical trials are essential in discovering whether new healthcare interventions improve outcomes for patients and the public. This distance learning programme will provide an excellent grounding in clinical trials and enhance the knowledge and understanding of those already working in the field. This is an expanding area that offers many exciting career opportunities.

UK tuition fees (2024/25)

Overseas tuition fees (2024/25), programme starts, applications accepted.

Applications open

• Entry requirements

Normally a minimum of an upper second-class UK Bachelor's degree in a healthcare or life science related subject (including pharmacy) or an overseas qualification of an equivalent standard. Clinicians are required to have a degree (for example, an MBBS).

The English language level for this programme is: Level 2

UCL Pre-Master's and Pre-sessional English courses are for international students who are aiming to study for a postgraduate degree at UCL. The courses will develop your academic English and academic skills required to succeed at postgraduate level.

Further information can be found on our English language requirements page.

Equivalent qualifications

Country-specific information, including details of when UCL representatives are visiting your part of the world, can be obtained from the International Students website .

International applicants can find out the equivalent qualification for their country by selecting from the list below. Please note that the equivalency will correspond to the broad UK degree classification stated on this page (e.g. upper second-class). Where a specific overall percentage is required in the UK qualification, the international equivalency will be higher than that stated below. Please contact Graduate Admissions should you require further advice.

About this degree

Clinical trials are essential in discovering whether new healthcare interventions improve outcomes for patients and the public. This is an expanding field that offers exciting career opportunities.

This online programme will provide an excellent grounding in clinical trials to those new to the field. It will enhance the knowledge and understanding of those already working in clinical trials.

Assessment and learning activities facilitate the development of key skills for careers or further study in the field, from analysis of scientific papers, the ability to critically challenge current research, to academic writing and oral presentation skills.

If you wish to gain a Master's award, you will undertake an independent research project, gaining experience of project design, literature review, analysis, and interpretation.

Who this course is for

The programme is aimed at graduates from healthcare, life sciences or other related disciplines and health professionals who are interested in a career in clinical trials. It is also aimed at professionals working in the field who wish to develop their knowledge and skills.

What this course will give you

The Institute of Clinical Trials and Methodology (ICTM) at UCL is a global leader in the field with over 450 researchers (including clinicians, statisticians, trials managers) working within it. You will meet and be taught by many of these researchers.

You will learn the scientific, methodological, and practical issues involved in the design, conduct, analysis, and reporting of clinical trials. You will learn about all types of trials, from early to late phase trials, and from simple to complex interventions. You will develop your communication skills through activities carried out both individually and in groups.  

The foundation of your career

Clinical trials is an expanding and highly competitive field of research yet employers find it challenging to recruit people with the appropriate skills and knowledge. This programme has been designed in consultation with employers from academia, the pharmaceutical industry and the NHS. It will give graduates the critical thinking, problem-solving and practical skills that employers seek in this multidisciplinary, collaborative field. You may also use this qualification as a springboard for further study at doctoral level. Future career prospects will be enhanced on completion of this programme. You will be equipped with the knowledge and skills to become a key team member in the design, conduct, analysis, and reporting of high-quality clinical trials.

Although I was already working in the field for 2 years, having career switched from organic chemistry, the MSc provided a strong theoretical and academic background that I was lacking in clinical and medical research. In addition, the degree also focuses on the 'nuts-and-bolts' involved in running a trial so being able to bounce off practical questions to colleagues on the course and tutors was equally invaluable. David Clinical Trials MSc Read more

Employability

Potential career opportunities include working on a range of trials from set up to final reporting.

Skills gained from the core programme will create exciting opportunities to work both in clinical trials and data management, regulation of clinical trials and medical writing.

Career destinations will include academic trials units, the pharmaceutical industry, contract research organisations, hospitals and government organisations.

You will be invited to the Institute’s Monday lunchtime seminars (1-2 pm UK time) which are hosted online on MS Teams. These seminars run throughout the academic year and feature invited speakers presenting on topics related to clinical trials / other research and initiatives relevant to staff and students in the Institute.  Students also have the opportunity to work with staff to set up an ICTM journal club – we will welcome volunteers to lead on this initiative each year. In 2023/24, we aim to set up UCL’s first Society for Online Students, giving online students the opportunity to network and make connections. 

Teaching and learning

As this is a distance learning programme, teaching will be delivered online in real-time and complimented with pre-recorded sessions. The students are expected to supplement these with self-study.

You will be assessed by a variety of methods including:

• Unseen written examinations
• Oral presentations
• Written assignments (for example, essays, abstracts, background section of a protocol, critical analysis of published work, practical problem solving, communicating appropriately with different audiences).

There are 7 core taught modules within this programme. The assessments will consist of a variety of formative assessments across the programme to facilitate learning outcomes within a module. These are aimed to help you prepare for the module’s summative assessment or to help develop key transferable skills.

Most of the taught modules are based on one summative assessment, while some have two summative assessments worth 50% each.

Assessments are based on real-world examples and activities that you would perform or need to be aware of if you work in clinical trials.

The overall contact and self-directed study hours are 150 hours for a typical 15-credit module (which includes 3 hours live online seminars per week).

A Postgraduate Diploma, consisting of seven core modules (120 credits) and available for full-time, part-time or flexible study is offered. A Postgraduate Certificate consisting of three or four modules (60 credits) and available for full-time, part-time and flexible study is offered.

Full-time students are expected to attend full-day online classes both on Tuesdays & Thursdays.

Part-time students have the flexibility to decide which modules they wish to undertake in that particular term/academic year, with classes either being on Tuesdays or Thursdays depending on your module selection. 

We encourage the students to take the Thursday modules in the first year and Tuesday modules in the second year.

Modular/flexible students have the flexibility to decide which modules they wish to undertake in that particular term/academic year. The choice of studying modules on Tuesdays or Thursdays will depend on the student's other commitments. The programme will need to be completed within the 5-year timeframe. 

Compulsory modules

Please note that the list of modules given here is indicative. This information is published a long time in advance of enrolment and module content and availability are subject to change. Modules that are in use for the current academic year are linked for further information. Where no link is present, further information is not yet available.

Students undertake modules to the value of 180 credits. Upon successful completion of 180 credits, you will be awarded an MSc in Clinical Trials. Upon successful completion of 120 credits, you will be awarded a PG Dip in Clinical Trials. Upon successful completion of 60 credits, you will be awarded a PG Cert in Clinical Trials.

Accessibility

Details of the accessibility of UCL buildings can be obtained from AccessAble accessable.co.uk . Further information can also be obtained from the UCL Student Support and Wellbeing team .

4 March 2024 — 30 August 2024

Online - Open day

Book a virtual 1-2-1 about Clinical Trials MSc

10:00 — 18:00

Book a 15-minute appointment with a member of the Clinical Trials MSc team. They will be happy to answer any questions you might have about the programme, careers or studying at UCL.

Book a virtual 1-2-1 about Statistics for Clinical Trials MSc

09:00 — 19:00

Book a 15-minute appointment with a member of the Statistics for Clinical Trials MSc team. They will be happy to answer any questions you might have about the programme, careers or studying at UCL.

Fees and funding

Fees for this course.

The tuition fees shown are for the year indicated above. Fees for subsequent years may increase or otherwise vary. Where the programme is offered on a flexible/modular basis, fees are charged pro-rata to the appropriate full-time Master's fee taken in an academic session. Further information on fee status, fee increases and the fee schedule can be viewed on the UCL Students website: ucl.ac.uk/students/fees .

Additional costs

There are no additional costs for this programme.

For more information on additional costs for prospective students please go to our estimated cost of essential expenditure at Accommodation and living costs .

Funding your studies

For a comprehensive list of the funding opportunities available at UCL, including funding relevant to your nationality, please visit the Scholarships and Funding website .

Students are advised to apply as early as possible due to competition for places. Those applying for scholarship funding (particularly overseas applicants) should take note of application deadlines.

There is an application processing fee for this programme of £90 for online applications and £115 for paper applications. Further information can be found at Application fees .

When we access your application we would like to learn:

• why you want to study Clinical Trials at graduate level
• why you want to study Clinical Trials at UCL
• what particularly attracts you to the chosen programme
• how your academic and professional background meets the demands of this challenging programme
• where you would like to go professionally with your degree

Together with essential academic requirements, the personal statement is your opportunity to illustrate whether your reasons for applying to this programme match what the programme will deliver.

Applications will be considered in gathered fields. For more information, please contact the ICTM administrator.

Please note that you may submit applications for a maximum of two graduate programmes (or one application for the Law LLM) in any application cycle.

Choose your programme

Please read the Application Guidance before proceeding with your application.

Year of entry: 2024-2025

Got questions get in touch.

Institute of Clinical Trials and Methodology

[email protected]

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