On November 30, 2018 Forbius, a clinical-stage company developing biologics for the treatment of cancer and fibrosis, reported that its collaborators at the Icahn School of Medicine at Mount Sinai will present a poster tomorrow, Dec. 1, featuring AVID200, at the 60th ASH (Free ASH Whitepaper) Annual Meeting (Press release, Forbius, NOV 30, 2018, View Source [SID1234531778]).
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Previous studies have shown that hyperactive TGF-beta signaling is a fundamental defect driving bone marrow fibrosis (Chagraoui et al., Blood, 2002). This presentation highlights the ability of AVID200 to shut down TGF-beta signaling, which decreases proliferation of mesenchymal stem cells and their collagen production. Importantly, when cells from myelofibrosis patients were treated with AVID200, this promoted proliferation of normal hematopoietic progenitors, while decreasing the proportion of myelofibrosis malignant progenitor cells.
AVID200 is uniquely positioned to be an effective treatment of MF because of isoform selectivity. TGF-beta 2 has been shown to be a positive promoter of hematopoiesis as well as normal cardiac function, whereas TGF-beta 1 and 3 promote fibrosis and myeloproliferation. AVID200 was therefore designed to selectively neutralize TGF-beta 1 & 3 for optimal efficacy and safety.
A Phase 1 trial evaluating AVID200 in patients with myelofibrosis is planned for early 2019.
The poster, entitled AVID200, a Potent Trap for TGF-β Ligands Inhibits TGF-β 1 Signaling in Human Myelofibrosis, will be presented by Lilian Varricchio, PhD, on Saturday, December 1st from 6:15 PM-8:15 PM PST in Hall GH of the San Diego Convention Center.
The abstract and full details for the poster presentation can be found on the ASH (Free ASH Whitepaper) website.
About AVID200
Forbius developed AVID200 to be a highly potent and isoform-selective TGF-β inhibitor. AVID200 neutralizes TGF-beta 1 and 3 with pM potency. These isoforms are known to be drivers of fibrosis and tumor immune resistance. In contrast, TGF-beta 2 is a positive regulator of hematopoiesis and normal cardiac function, therefore blockade of TGF-beta 2 is undesirable. The ability of AVID200 to selectively target TGF-beta 1 and 3 positions it to be an effective and well-tolerated therapeutic in fibrotic diseases and immune oncology.