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Clinical Trials

Date: 2018-11-03

Type of information: Presentation of results at a congress

phase: preclinical

Announcement: presentation of results at Neuroscience 2018

Company: Disarm Therapeutics (USA - MA)

Product: SARM1 inhibitor

Action mechanism: SARM1 inhibitor

Disease:

Therapeutic area: Neurological diseases - Neurodegenerative diseases

Country:

Trial details:

Latest news:

  • • On November 3, 2018, Disarm Therapeutics announced data demonstrating that genetic inhibition of SARM1 prevents axonal degeneration in the central, ocular and peripheral nervous systems. Disarm also discovered that SARM1 inhibition lowers two biomarkers – blood NF-L and cADPR – providing critical insight into the development of small-molecule inhibitors of SARM1, identified by Disarm’s scientific founders as the central driver of axonal degeneration. These data are presented as a scientific poster at the Neuroscience 2018 conference in San Diego.
  • Highlights from the data presented at Neuroscience 2018 include:
  • -SARM1 genetic deletion protects axons in vitro and in vivo
  • -cADPR, a metabolite of SARM1, was identified, for the first time, as a proximal biomarker of SARM1 enzymatic activity in vitro and in vivo
  • -NF-L, a prognostic biomarker of neurodegeneration increasingly used in the clinic, is released in blood following CNS, ocular, and PNS axonal degeneration in a SARM1-dependent manner.
  • • On July 23, 2018, Disarm Therapeutics presented data demonstrating SARM1 deletion prevents axonal degeneration following traumatic and chemical nerve injuries. The data also show, for the first time, that in vitro and in vivo release of NF-L, an increasingly used clinical biomarker of axonal degeneration, is SARM1-dependent.
  • The SARM1 protein was identified by Disarm’s scientific founders as the central driver of axonal degeneration. The company is developing inhibitors of SARM1 to prevent axonal degeneration in chronic and acute diseases of the central, ocular, and peripheral nervous systems.
 

Is general: Yes