REHOVOT, Israel, Sept. 20, 2021 /PRNewswire/ — BASED OF THE SATISFACTORY SAFETY DATA OF VIDAC VDA 1102 ON SELECTED PATIENTS VIDAC PHARMA RECEIVED AUTHORIZATION TO WIDEN THE SCOPE OF THE TRIAL TO CTCL WHOLE SPECTRUM OF CONDITIONS.
«WE ARE VERY SATISFIED WITH THE RESULTS OF THE FIRST STEP WHICH ON TOP OF THE SAFETY RESULTS GRANTED TO OUR TRIAL A DOSE RANGING PROTOCOL AUTHORIZATION. THIS WILL ALLOW US TO SPEED UP RECRUITMENT AT BEILINSON HOSPITAL IN ISRAEL UNDER THE DIRECTION OF PROF EMILIA HODAK AND PROGRAM A PHASE 2B BOTH IN ISRAEL AND IN EUROPE. IN A PRE-APPROVAL MEETING THE AUSTRIAN HEALTH AUTHORITIES (AGES) FOUND OUR PLANNING SATISFACTORY AND RECOMMENDED SUCH AN EXTENSION TO THE FULL SPECTRUM,» DECLARED DR MAX HERZBERG VIDAC PHARMA CHAIRMAN.
VDA 1102 DISRUPTS THE BINDING OF HEXOKINASE 2 (HK2) WHICH IS OVER EXPRESSED IN CANCER CELLS AND BINDS TO THE VDAC CHANNEL OF MITOCHONDRIA. THIS BINDING CAUSES EXAGGERATED GLYCOLYSIS AND BLOCKS APOPTOSIS. THE EXTREMELY SPECIFIC DISPLACEMENT OF HK2 BRINGS BACK METABOLISM TO THAT OF A NORMAL CELL AND CORRECTS TUMOR MICROENVIRONMENT. THE COMPANY SEES THIS MECHANISM OF «TOPOSTERIC EFFECT TM» AS A NOVEL TARGET TO CREATE SAFER PHARMACOLOGICAL ENTITIES.
Vidac Pharma was founded in Israel in 2012 by Dr Max Herzberg and aims to develop anti-cancer drugs based on restoring normal cellular metabolism. Cancer cells are characterized by a high rate of glycolysis and by suppressed apoptosis (programmed death) both of which favorizes high cellular reproduction and Tumor formation. Vidac’s platform technology restores normal glycolysis and triggers apoptosis in these malignant cells. As normal cells are not subject to overexpression of HK2 they are not affected by Vidac’s drugs. Vidac’s lead drug, VDA-1102, has successfully completed a Phase 2b clinical trial in actinic keratosis (AK) under an IND from the FDA and is presently in a Phase 2a clinical trial in CTCL in Israel. The company’s strategic intellectual property portfolio covers broadly its general approach using the TopostericTM effect avoiding enzymatic cell mis-location.