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The Global Cachexia Pathway Navigating from Early Recognition to Therapeutic Horizons: Module 3 Translating Emerging Cachexia Science

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Description

This program is supported by an independent education grant from Pfizer. This education program is available to healthcare professionals globally.

Credits: 0.25 AMA PRA Category 1 Credits™ (0.25.00 hours)

Type of activity: Enduring material (On-demand)

Launch date: September 28th 2026

Expiration date: March 1st 2028

Estimated time to complete this activity: 15 minutes

Prefer to read instead? Read our Key Clinical Summaries in your preferred language:

This is Module 3 of a three-part on-demand series: Module 1 and Module 2.

Activity Description

Join expert Dr Richard Dunne, MD, for an engaging exploration of the emerging science shaping the future of cancer cachexia management. This case-based session examines the biology of GDF-15 and its role in appetite dysregulation and cachexia progression, alongside emerging targeted approaches designed to address the underlying mechanisms of the syndrome. Participants will explore evolving clinical evidence, consider the potential role of biomarker-driven treatment strategies, and learn how to identify appropriate patients for cachexia-focused clinical trials. The session will also highlight how emerging therapies may complement — rather than replace — the foundations of multimodal supportive care.

Session Highlights

Explore the role of GDF-15 and GFRAL signalling in appetite loss and cachexia progression.
Examine emerging evidence for targeted and biomarker-driven approaches to cancer cachexia.
Understand how investigational therapies could complement established nutritional, exercise, and symptom-management strategies.
Identify patients who may be appropriate for cachexia-focused clinical trials and recognise the importance of early referral.

Who Should Participate?

This program is designed for healthcare professionals directly involved in the diagnosis, treatment, supportive management, and longitudinal follow-up of people with cancer across oncology care settings, who seek to strengthen their recognition and management of cancer cachexia and incorporate earlier assessment and multidisciplinary support into routine clinical practice.

Medical Oncologists
Oncology Nurses
Nurse Practitioners
Physician Associates/Assistants
Pharmacists
Dietitians/Nutrition Specialists
Supportive Care and Palliative Care Clinicians
Rehabilitation and Physical Therapy Professionals
Other Multidisciplinary Cancer Care Team Members

Faculty

Dr Richard Dunne

Dr Richard Dunne is an Associate Professor of Medicine in Hematology/Oncology at the University of Rochester Medical Center, with a research focus on cancer cachexia, sarcopenia, and supportive care. His work explores the impact of weight loss, muscle wasting, nutritional impairment, and physical function on outcomes for patients with cancer, particularly older adults. Dr Dunne is committed to advancing the understanding and management of cancer cachexia through translational research and clinical trials, with the goal of improving quality of life, treatment tolerance, and outcomes for patients with advanced cancer.

Continuing Education Information

Commercial support: This activity received monetary support through an independent education grant from Pfizer.

This continuing education activity will be provided by AffinityCE and MedAll. This activity will provide continuing education credit for physicians. A statement of participation is available to other attendees.

Disclosures

Dr Richard Dunne has disclosed financial relationships within the past 24 months with the following ineligible companies: Executive Steering Committee Member, Pfizer. Advisory Board, Eisai, Incyte. Dr Dunne does intend to discuss non-FDA uses of drug products: Ponsegromab, Visugromab. Dr Dunne will disclose to the audience when this discussion takes place.

AffinityCE staff, MedAll staff, as well as planners and reviewers, have no relevant financial relationships with ineligible companies to disclose.

Mitigation of Relevant Financial Relationships

AffinityCE adheres to the ACCME’s Standards for Integrity and Independence in Accredited Continuing Education. Any individuals in a position to control the content of a CME activity, including faculty, planners, reviewers, or others, are required to disclose all financial relationships with ineligible companies. All relevant financial relationships for anyone associated with the content of this activity were mitigated prior to the release of this program.

Activity Accreditation for Health Professions

Physicians

This enduring material has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Physician Assistants

This enduring material has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credits™. Physician assistants should claim only the credit commensurate with the extent of their participation in the activity.

Nurse Practitioners

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credits™. Nurse practitioners should claim only the credit commensurate with the extent of their participation in the activity.

Nurses & Other Professionals

All other health care professionals completing this continuing education enduring material will be issued a statement of participation indicating the number of hours of continuing education credit. This may be used for professional education CE credit. Please consult your accrediting organization or licensing board for their acceptance of this CE activity.

System Requirements

Mobile device (e.g., large-format smart phone; laptop or tablet computer) or desktop computer with a video display of at least 1024 × 768 pixels at 24-bit color depth, capable of connecting to the Internet at broadband or faster speeds, with a current version Internet browser and popular document viewing software (e.g., Microsoft Office, PDF viewer, image viewer) installed. Support for streaming or downloadable audio-visual materials (e.g., streaming MP4, MP3 audio) in hardware and software may be required to view, review, or participate in portions of the program.

Unapproved and/or off-label use disclosure

AffinityCE/MedAll requires CE faculty to disclose to the participants:

When products or procedures being discussed are off-label, unlabeled, experimental, and/or investigational (not US Food and Drug Administration [FDA] approved); and
Any limitations on the information presented, such as data that are preliminary or that represent ongoing research, interim analyses, and/or unsupported opinion.

CME Inquiries

For all CME policy-related inquiries, please contact us at ce@affinityced.com.

Participation Costs

There is no cost to participate in this program.

This continuing education activity is active starting September 28th 2026, and will expire on March 1st 2028.

Estimated time to complete this activity: 15 minutes.

Learning objectives

Implement standardized assessment and documentation strategies to identify cancer cachexia earlier in patients with weight loss, muscle wasting, and functional decline: ➔ Apply consensus diagnostic criteria and structured cachexia screening approaches in oncology practice. ➔ Differentiate cachexia from sarcopenia, malnutrition, and treatment-related weight loss. ➔ Integrate assessment and documentation of weight loss, appetite, muscle mass, and functional status into routine patient evaluation.
Integrate evidence-based multimodal supportive care strategies into management plans for patients with cancer cachexia to improve appetite, physical function, lean body mass, and treatment tolerance: ➔ Apply nutritional, rehabilitative, pharmacologic, and symptom-management approaches within multidisciplinary oncology care. ➔ Align supportive care interventions with patient functional status and anticancer treatment goals. ➔ Incorporate earlier supportive intervention strategies into routine oncology workflows.
Apply emerging evidence on GDF-15 biology and investigational cachexia therapies when evaluating patients for clinical trial opportunities: ➔ Recognize the mechanism of GDF-15 in appetite dysregulation, metabolic dysfunction, and cancer cachexia progression. ➔ Interpret evolving evidence on targeted therapies and biomarker-driven approaches in cancer cachexia, including the latest trials evaluating the GDF-15–GFRAL pathway as well as other pathways. ➔ Identify patients who may be appropriate for cachexia-focused clinical trials and emerging therapeutic strategies.

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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hi, my name is Doctor Richard Dunn, and I'm an associate professor of medicine and a medical oncologist at the Wilmot Cancer Institute at the University of Rochester Medical Center in New York. Before I begin, here are my disclosures. And for my portion, I'd like to go over some learning objectives. The first to recognize the mechanism of growth differentiation factor 15 or GDF 15. In appetite dysregulation and cachexia progression. The second, to interpret evolving evidence on different targeted and biomarker driven approaches in cancer cachexia. And 3, discuss how we may identify patients who may be appropriate for cachexia-focused clinical trials. So Cachexia historically is an under-recognized and understudied uh syndrome. And uh there are several reasons for that. Um, I think over the years, there have been several different definitions of what cachexia is, which can kind of get uh confusion, uh confusing. There's a different lexicon of, of different terms used to describe weight loss and muscle loss, uh, in cancer. There hasn't really been a standard treatment, uh, and historically some have looked at, uh, cachexia as kind of an end-stage process with no available treatment. Uh, but we're learning more about this, and we're learning that cachexia is actually happening. Uh, early on in the diagnosis, and a lot of the focus has turned to early recognition and where we think intervention may be more effective. So, um, you know, there certainly is a knowledge gap. I think the, the understanding of cachexia, um, has improved over the last 5 to 10 years, uh, but this knowledge gap among clinicians. Uh, still exists. Um, there's also a knowledge gap in terms of, uh, how do I find a cachexia trial, uh, for my patients, uh, what may be the eligibility criteria. You may never have enrolled a patient on a cachexia trial, uh, before because they have been very limited in the past, and now we have the emergence of multiple, uh, early stage but also late phase, phase 2 and phase 3 trials. Um, there are currently no agents approved for cancer cachexia in the US or European Union, and we're hoping that changes in the years to come. So, uh, we'll revisit the case of, uh, Mr. A. So this is one of our polling questions. So Mr. A's serum GDF 15 level is markedly elevated. Through which mechanism does GDF 15 most directly drive his loss of appetite? Is it A, activating the ubiquitin proteosome system in skeletal muscle? Is it B, binding Gfrau in the hindbrain, driving Aversive appetite suppression, is it C inhibiting ghrelin at the growth hormone secretagogue receptor? Is it D signaling through activin type 2 receptors on myocytes, or E blocking melanocortin 4 receptors in the hypothalamus? So the correct answer is actually B. So GDF 15 acts centrally by binding its receptor, GRAL, which is a receptor whose expression is essentially restricted to the area of post strama and uh in the hindbrain. And these other uh answer choices here are uh other uh mechanisms that have been um developed uh in uh pre-clinical work and also been targeted uh in clinical trials, um, ubiquitin proteasome, uh. Inhibiting ghrelin is a target that has been explored in clinical trials, and the drug enamellin, which targets ghrelin, is approved in Japan for cachexia and active in type 2 is working directly on muscle, and melanocortin 4 is another pathway that focuses on appetite suppression in the brain. So let's talk a little bit more about GDF 15, um, and kind of the, the mechanism and pathway of how it may, uh, drive, uh, the change in eating amongst our patients. So GDF 15 is thought to be a stress hormone or stress cytokine, uh, that is released under inflammatory stress. Uh, tumors overexpress GDF-15. Um Patients who receive chemotherapy will have elevation in their GDF-15, particularly platinum chemotherapies. So circulating GDF-15 will rise in certain situations like cancer and people receiving chemotherapy, and greater GDF-15 levels is associated with weight loss, uh, and worse prognosis in patients with cancer. The rise in GDF-15 will lead to GDF-15 binding to its receptor GRAL in the hindbrain, and this drives anorexia, nausea, vomiting, and aversion to certain foods. So, um, this GDF-15 over the last few years has emerged as a very attractive target in cachexia. Gfrau is largely confined to the hindbrain, um, and blocking it in pre-clinical studies and early clinical trials has shown to be relatively safe. There also is a way to detect GDF-15 levels in the blood so it can serve as a biomarker. It's measurable and also prognostic and has been used as an entry criteria for some clinical trials. This is not something that you can test for in your clinic just yet. It's not validated. We're still trying to learn what proper thresholds of what. GDF 15 levels should be normal and what should be elevated. Uh, so currently checking it outside of a trial doesn't really change, uh, management, but there is. Work that's being done. To try to develop this as a serum biomarker that may be more available to clinicians. So, uh, this slide here, uh, summarizes a phase 2 trial, uh, evaluating an anti-GDF 15 antibody, uh, poonsagrimab, uh, versus placebo. Uh, this was published in the New England Journal of Medicine in 2024. 187 patients with lung, pancreatic, and colorectal cancer, uh, were randomized to either 3 different doses of poonsagrimab, uh, or placebo. Um, The bar graph on the, on the left, uh, shows that there was a dose response. So with higher doses of ponsagumab, uh, there was greater weight gain. So, uh, weight gain was the primary endpoint here. And higher doses of pomab were more effective at weight gain compared to placebo. Other things that were seen were appetite and cachexia symptoms improved. There was an improvement in non-sedentary physical activity. We saw skeletal muscle index improve, and again there was a good safety profile. So, uh, this phase 2 study, um, was the basis for, um, a phase 3 trial, uh, that is ongoing. So GDF 15 is, is one target among several, and there are multiple other pathways that are in development, uh, again, both in pre-clinical work as well as, uh, um, emerging clinical trials. So, uh, targets, uh, going after appetite like GDF 15, um, and melanocortin 4, which was mentioned in the, in the poll question earlier, uh, as well as, uh, targeting ghrelin. Uh, there are, um, There are pathways looking to target muscle metabolism. Both myostatin and active in A bind to the same receptors, active in type 2.