Profile of panobinostat and its potential for treatment in solid tumors: an update

Madhurima Anne1, Daniel Sammartino, Myra F Barginear

  • 1Monter Cancer Center, Hofstra North Shore-LIJ School of Medicine, Lake Success, NY, USA.

Oncotargets and Therapy
|November 23, 2013
PubMed

Insights

Panobinostat, a potent histone deacetylase (HDAC) inhibitor, shows promise in cancer therapy by inhibiting cell proliferation and inducing apoptosis. Its efficacy in solid tumors is under investigation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Histone deacetylase (HDAC) inhibitors are emerging as novel cancer therapies.
  • Panobinostat (LBH 589) is a pan-deacetylase inhibitor evaluated in various formulations and tumor types.

Purpose of the Study:

  • To review the current status of panobinostat.
  • To discuss the role of panobinostat in treating solid tumors.

Main Methods:

  • Review of preclinical data on panobinostat's efficacy.
  • Analysis of panobinostat's mechanism of action, including histone hyperacetylation and apoptosis induction.
  • Evaluation of clinical trial data for panobinostat in solid tumors.

Main Results:

  • Panobinostat induces hyperacetylation of histones and other proteins, leading to repressed gene expression, inhibited cellular proliferation, and apoptosis.
  • Panobinostat activates cellular death receptor pathways, contributing to apoptosis.
  • Preclinical data indicate potent inhibitory activity at nanomolar concentrations, positioning it as a highly potent HDAC inhibitor.

Conclusions:

  • Panobinostat demonstrates significant preclinical potency and a dual mechanism for inducing cancer cell death.
  • Further investigation into panobinostat's role in solid tumor treatment is warranted.

Related Concept Videos

Treatment Resistent Cancers02:56

Treatment Resistent Cancers

1.1K
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...
2.7K
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...
7.1K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

1.5K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.5K