Related Experiment Video

Updated: Apr 11, 2026

Transarterial Administration of Oncolytic Viruses for Locoregional Therapy of Orthotopic HCC in Rats
08:55

Transarterial Administration of Oncolytic Viruses for Locoregional Therapy of Orthotopic HCC in Rats

Published on: April 15, 2016

10.0K

Tivantinib (ARQ197) in hepatocellular carcinoma

Camillo Porta1, Palma Giglione, Alessandra Ferrari

  • 1Medical Oncology, I.R.C.C.S. San Matteo University Hospital Foundation, Pavia, Italy.

Expert Review of Anticancer Therapy
|June 3, 2015
PubMed

Insights

Tivantinib, a c-MET inhibitor, shows promise in treating advanced liver cancer. It improved survival and slowed progression in patients with MET-high hepatocellular carcinoma after sorafenib treatment.

Area of Science:

  • Oncology
  • Pharmacology

Background:

  • Hepatocellular carcinoma (HCC) remains a significant health challenge.
  • Sorafenib is a standard treatment, but resistance and progression are common.
  • Targeting the c-MET pathway is a potential therapeutic strategy for HCC.

Purpose of the Study:

  • To review the development of tivantinib, a selective oral c-MET inhibitor.
  • To evaluate the efficacy and safety of tivantinib in patients with advanced HCC who progressed on sorafenib.

Main Methods:

  • Review of tivantinib's development and clinical trial data.
  • Analysis of a randomized Phase II study in HCC patients post-sorafenib.
  • Assessment of overall and MET-high patient populations.

Main Results:

  • Tivantinib (360 mg BID) reduced progression risk by 36% in the overall HCC population.
  • In MET-high HCC patients, tivantinib significantly improved overall survival, time to progression, and disease control rate.
  • Dose reduction to 240 mg BID mitigated neutropenia without compromising efficacy.

Conclusions:

  • Tivantinib demonstrates clinical activity in advanced HCC, particularly in MET-high patients.
  • The drug's safety profile, including neutropenia, can be managed with dose adjustments.
  • Ongoing Phase III trials will further validate tivantinib's role in HCC treatment.
Keywords:
MET inhibitordevelopmenthepatocellular carcinomativantinib

More Related Videos

Y-90 Radioembolization and PD-1 Inhibitor as Neoadjuvant Treatment in Hepatocellular Carcinoma09:11

Y-90 Radioembolization and PD-1 Inhibitor as Neoadjuvant Treatment in Hepatocellular Carcinoma

Published on: May 24, 2024

1.5K
Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma06:15

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma

Published on: October 27, 2014

28.0K

Related Concept Videos

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...
9.2K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

1.8K
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

1.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.4K
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
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...
778