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August 01, 2015 2:58 AM ET


Company Overview of Tensha Therapeutics, Inc.

Company Overview

Tensha Therapeutics, Inc. develops anti-cancer compound for curing acute myeloid leukemia. The company was incorporated in 2011 and is based in Cambridge, Massachusetts.

55 Cambridge Parkway

Suite 102

Cambridge, MA 02142

United States

Founded in 2011



Key Executives for Tensha Therapeutics, Inc.

President and Director
Age: 46
Compensation as of Fiscal Year 2015.

Tensha Therapeutics, Inc. Key Developments

Tensha Therapeutics Announces First Clinical Trial of BET Bromodomain Inhibitor TEN-010 for Treatment of Cancer

Tensha Therapeutics announced that it has begun the first clinical trial of its small molecule, bromodomain and extra-terminal domain (BET) bromodomain inhibitor, TEN-010 for the treatment of cancer. The trial is designed to assess the safety, tolerability and anti-tumor activity of TEN-010 in patients with advanced solid tumors that are refractory or intolerant to standard/approved therapies and NUT midline carcinoma (NMC), a highly aggressive cancer with very limited treatment options. Bromodomains, which are modules contained within epigenetic proteins, play critical roles in influencing gene transcription by functioning as 'readers' of epigenetic marks. Once bound to chromatin, these bromodomain-containing proteins can influence gene expression. Tensha's Founder, James Bradner, MD, an Assistant Professor at Harvard Medical School and Investigator at the Dana-Farber Cancer Institute, was the first to recognize the broad potential of small molecule BET bromodomain inhibitors across a range of therapeutic areas. Dr. Bradner's seminal work identified NMC as sensitive to BET bromodomain inhibition. NMC is a rare, invariably fatal cancer caused in the majority of cases by a gene translocation event that results in the expression of the NUT protein fused to the BET bromodomains of BRD3 or BRD4. Subsequent studies from Dr. Bradner's and collaborating laboratories have established BET bromodomain inhibition as a therapeutic strategy to target Myc overexpression and demonstrated the potential of this approach to other cancers, including multiple myeloma, acute myeloid leukemia, non-small cell lung cancer and neuroblastoma.

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