INTRODUCING OUR LEAD ASSET

Vensobafusp alfa (KP104)

The first bifunctional biologic in complement.

Our lead program, KP104 represents a significant breakthrough in complement therapy. It is a potent, first-in-class bifunctional biologic designed to simultaneously and selectively block the alternative and terminal pathways, providing a powerful and synergistic method of targeting validated drivers of complement disease.

Safety Data

Data to date suggests strong safety across SAD and MAD, with no clinically relevant safety findings or signs of immunogenicity.

Orphan Drug Designation

KP104 was recently granted Orphan Drug Designation by the U.S. FDA for the Treatment of Paroxysmal Nocturnal Hemoglobinuria (PNH).

Multiple Formulations and Good Manufacturing Data

KP104 has a formulation suitable for both intravenous and subcutaneous administrations. Initial manufacturing experience demonstrates high yield manufacturing and high purity.

Enhanced Inhibition of AP and TP

KP104 has been engineered to have an extended half-life and high potency. Its Factor H domain provides proximal complement inhibition at the C3 convertase step of the alternative pathway amplification loop while the anti-C5 antibody moiety provides inhibition of the terminal pathway and also acts as a tissue targeting device to bring Factor H regulatory function to tissues with C5b-9 deposition by virtue of its C5b-binding activity.

MECHANISM OF ACTION

KP104 Targets Multiple Pathways

KP104 is the only drug to simultaneously block the upstream Alternative Pathway (Factor H) and downstream Terminal Pathway (C5). With this novel dual-approach mechanism of action, KP104 is uniquely positioned to target complement-mediated diseases where single-target C5 or C3 inhibitors alone are inadequate.

Recently, evidence has emerged to suggest that for certain indications, such as PNH, simultaneous blockade of both proximal and terminal complement pathways may be needed. Click here to read the NEJM paper.

In the case of PNH, C5 inhibition treats intravascular hemolysis (IVH), but the alternative pathway is unchecked and can cause extravascular hemolysis (EVH) and no amount of C5 inhibition will treat EVH. Thus, PNH patients treated with only a C5 inhibitor require ongoing transfusions and have reduced quality-of-life. On the other hand, proximal complement inhibitors can stop EVH and this will lead to accumulation of PNH clones, in some cases up to 95-99%. See Blood Paper. The latter outcome, when coupled to a pharmacokinetic breakthrough of the proximal inhibitor, may produce more severe and life-threatening intravascular hemolysis. See the NEJM paper. A potential solution to this clinical challenge in PNH management may be combinatorial usage of proximal and terminal complement inhibitors, but cost and patient compliance could be a major hurdle for such an approach. Involvement of multiple pathways of complement activation may not be restricted to PNH and it is likely that other complex complement-mediated diseases could have similar pathogenic mechanisms. As the first and only bifunctional complement inhibitor, KP104 is uniquely suited to address the inadequacy of single pathway complement inhibitors, both in efficacy and patient compliance.

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Jasper Therapeutics and Kira Pharmaceuticals
Announce Merger Agreement

Read press release Visit Kira Pharma website