Kahr has raised $46.5 million to move a CD47x4-1BB targeting fusion protein deeper into the clinic. The size of the financing leaves Kahr with enough money left over to take a TIGITxPD-1 asset through IND-enabling studies.
Jerusalem-based Kahr reeled in $18 million last year to fund early-phase development of lead drug DSP107, which is designed to simultaneously block an immunosuppressive signal and activate T cells by binding to CD47 and 4-1BB. DSP107 is now in a phase 1/2 clinical trial that is testing it as a single agent and in combination with Roche’s Tecentriq in patients with advanced solid tumors.
Kahr sees particular potential for DSP107, as a monotherapy and in combinations, in patients with non-small cell lung cancer, the focus of the second part of the clinical trial. The biotech also plans to start a phase 1/2 clinical trial in acute myeloid leukemia, myelodysplastic syndrome and T-cell lymphoproliferative diseases in the coming months. The trial will test DSP107 in combination with azacitidine and venetoclax, the active ingredients in Vidaza and Venclexta, respectively.
An expanded syndicate of investors has come together to fund the work. The round was led by aMoon with the support of new investors BVF Partners, DAFNA Capital Management, Peregrine Ventures, Shavit Capital and the Cancer Focus Fund. Existing backers including Flerie Invest also returned for the latest round.
The expansion of the syndicate and dialing up of the fundraising haul equips Kahr to start a new trial of DSP107 while pushing other candidates toward the clinic. Kahr’s preclinical pipeline includes DSP502, a TIGITxPD-1 fusion protein.
GlaxoSmithKline cemented the status of TIGIT as a red-hot immuno-oncology target this week by agreeing to pay iTeos Therapeutics $625 million upfront for rights to phase 1 candidate. Companies including Merck and Roche are studying the use of anti-TIGIT antibodies in combination with PD-1/L1 checkpoint inhibitors. In DSP502, Kahr has a single molecule designed to hit both TIGIT and PD-1.
DSP502 is set to advance through IND-enabling studies alongside another preclinical asset, DSP216. The other candidate is a LILRB2xSIRPa fusion protein. LILRB2 could act as an immune checkpoint for macrophages and other myeloid cells. The SIRPa element of the molecule is designed to block CD47, thereby inhibiting the “don’t eat me” signal.