Development of Tivantinib as Treatment for Hepatocellular Carcinoma

Jennifer Au1, Catherine Frenette2

  • 1Division of Gastroenterology, Department of Medicine, Scripps Green Hospital, La Jolla, CA.

Insights

Tivantinib shows promise for treating advanced hepatocellular carcinoma (HCC) by targeting the c-Met pathway. This MET inhibitor improved time to progression in HCC patients with high c-Met activity.

Area of Science:

  • Hepatocellular carcinoma (HCC) research
  • Molecular oncology
  • Drug development

Background:

  • Hepatocellular carcinoma (HCC) is a leading cause of cancer death globally.
  • Advanced HCC often requires systemic therapy.
  • The c-Met pathway is implicated in HCC development and progression in about half of patients.

Purpose of the Study:

  • To evaluate tivantinib, a MET inhibitor, for HCC treatment.
  • To assess the efficacy and safety of tivantinib in HCC patients.
  • To investigate the role of c-Met pathway activation in HCC treatment response.

Main Methods:

  • Review of Phase I and II clinical trial data for tivantinib.
  • Analysis of patient outcomes in HCC, focusing on those with elevated c-Met activity.
  • Assessment of safety profile, including common side effects like neutropenia.

Main Results:

  • Tivantinib demonstrated an improved time to progression (2.7 months) compared to placebo (1.4 months) in HCC patients with elevated c-Met activity.
  • The drug exhibits a generally adequate safety profile.
  • Neutropenia was identified as a primary side effect.

Conclusions:

  • Tivantinib is a potential targeted therapy for HCC, particularly in patients with high c-Met pathway activation.
  • Further clinical studies are warranted to confirm its efficacy and safety.
  • Tivantinib warrants close attention as a future treatment option for HCC.

Related Concept Videos

Treatment Resistent Cancers02:56

Treatment Resistent Cancers

1.5K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.9K
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
562
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
9.1K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

1.8K
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
758