Related Experiment Video

Updated: May 13, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.5K

Larotrectinib-associated withdrawal symptoms resolved following initiation of GLP-1 receptor agonist: a case report

Reema Patel1, John F Deeken2

  • 1University of Pittsburgh Medical Center, Pittsburgh, PA, USA.

Cancer Chemotherapy and Pharmacology
|October 22, 2025
PubMed
Abstract

Insights

Tropomyosin receptor kinase (TRK) inhibitors can cause withdrawal-like symptoms. A patient with NTRK gene fusion cancer experienced relief from these side effects after starting semaglutide.

Area of Science:

  • Oncology
  • Pharmacology
  • Genetics

Background:

  • Tropomyosin receptor kinase (TRK) inhibitors are targeted therapies for tumors with NTRK gene fusions.
  • Withdrawal-like symptoms, including arthralgias, myalgias, and allodynia, affect about one-third of patients on TRK inhibitors.
  • These symptoms can occur with missed, delayed, or discontinued therapy.

Purpose of the Study:

  • To report a case of daily withdrawal-like symptoms in a patient treated with a TRK inhibitor.
  • To investigate the effect of semaglutide on these TRK inhibitor-associated side effects.

Main Methods:

  • A 35-year-old male with metastatic ETV6-NTRK3 fusion parotid gland cancer received larotrectinib.
  • The patient experienced daily myalgias, arthralgias, and light sensitivity before each dose.
  • Semaglutide, a GLP-1 receptor agonist, was initiated to manage these symptoms.

Main Results:

  • The patient experienced rapid and complete response to larotrectinib, continuing therapy for over seven years.
  • Withdrawal-like symptoms occurred twice daily, starting 30-45 minutes before the scheduled dose.
  • Initiation of semaglutide led to complete resolution of the patient's symptoms.

Conclusions:

  • GLP-1 receptor agonists may help manage side effects associated with TRK inhibitor therapy.
  • Further research is needed to explore the mechanisms behind this potential therapeutic effect.
Keywords:
CancerLarotrectinibMyalgiasSemaglutide

More Related Videos

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution04:14

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution

Published on: April 16, 2019

12.6K
Multidisciplinary Approach to Obesity Management: A Case Report05:10

Multidisciplinary Approach to Obesity Management: A Case Report

Published on: May 30, 2025

902

Related Concept Videos

Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists01:28

Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists

Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...
Drugs for Treatment of Diarrhea-Predominant IBS01:17

Drugs for Treatment of Diarrhea-Predominant IBS

Diarrhea-predominant irritable bowel syndrome (IBS-D) is a subtype of IBS characterized primarily by frequent, loose, or watery stools, abdominal pain, and abdominal discomfort. Therapeutic approaches to managing IBS-D include dietary changes, stress management techniques, and pharmaceutical interventions.
Two specific drugs used in the treatment are alosetron (Lotronex) and eluxadoline (Viberzi). Alosetron, a 5-HT3 antagonist, works by slowing the movement of stools in the gut, reducing bowel...
Drugs for Treatment of Constipation-Predominant IBS01:21

Drugs for Treatment of Constipation-Predominant IBS

Pharmacological therapies for IBS-C are designed to alleviate abdominal discomfort and enhance bowel function. In patients with IBS-C, fiber supplements may help soften stools and decrease straining, but may also lead to increased gas production and bloating. Osmotic laxatives like milk of magnesia are frequently used to soften stools and increase stool frequency in IBS-C patients. In addition, two drugs approved for use in severe IBS-C adult cases are linaclotide (Linzess) and lubiprostone...
Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...