- AVID200 potently shuts down TGF-beta signaling, inhibits proliferation of mesenchymal stem cells and their collagen production, and promotes growth of normal hematopoietic progenitor cells
- A Phase 1 clinical trial evaluating AVID200 in myelofibrosis planned for early 2019
- AVID200 presentation on Saturday, December 1st at 6:15 PM PST
(Nov. 30, 2018) – Forbius, a clinical-stage company developing biologics for the treatment of cancer and fibrosis, announced 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 Annual Meeting.
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 website.
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.
About Forbius: Targeting EGFR and TGF-β Pathways in Cancer and Fibrosis
Forbius is a clinical stage company that designs and develops biotherapeutics for the treatment of cancer and fibrotic diseases. We use our strength in biological understanding and diverse protein engineering technologies to design superior inhibitors of validated pathways. We have particularly deep expertise in targeting the transforming growth factor-beta (TGF-beta) and epidermal growth factor receptor (EGFR) pathways. For both of these pathways, there is a significant body of evidence validating their role as drivers of multiple life-threatening conditions, including cancer and fibrosis. However, in the case of the EGFR pathway, the majority of patients do not benefit from currently marketed EGFR inhibitors; in the case of the TGF-beta pathway, no agent targeting this pathway has yet been approved. By using multiple complementary platform technologies, Forbius’ team overcame barriers that prevented the development of effective therapeutics targeting these pathways.