Mirador licenses long-acting antibody therapy for AAV development
Phase 1 study is planned by year-end, followed by Phase 2 in 2027
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Mirador Therapeutics has secured worldwide development and commercialization rights to KP-301, an experimental long-acting antibody therapy licensed from Kira Pharmaceuticals, and plans to develop it for ANCA-associated vasculitis (AAV).
KP-301 is a long-acting antibody that blocks C5a, a protein in the complement system that helps drive inflammation and small blood vessel damage in AAV. It is designed to provide sustained C5a suppression with infrequent dosing, which Mirador says could support long-term treatment.
Complement pathway offers a treatment target
“The biology of complement-driven vascular [blood vessel] inflammation is well established, yet significant unmet need remains,” Mark C. McKenna, chairman and CEO of Mirador, said in a company press release. “KP-301 gives us the opportunity to deliver the benefit of C5a signaling [suppression] through a differentiated, long-acting antibody, and it expands our portfolio into inflammatory vascular disease, where the science, the modality and the unmet need clearly align.”
According to Mirador, a Phase 1 clinical trial of KP-301 is expected to begin by year’s end. The company plans to launch a Phase 2 trial in people with AAV in the first half of 2027.
AAV is typically caused by self-targeting antibodies, called ANCAs, that overactivate neutrophils, a type of immune cell. These immune cells, in turn, activate the complement cascade, a network of proteins that normally helps defend the body against infections, leading to the production of C5a.
C5a then binds to its receptor protein, C5aR, on neutrophils, further promoting their abnormal activation. This worsens inflammation and damage to the body’s small blood vessels, potentially affecting organs such as the kidneys, lungs, skin, and nerves.
The C5a/C5aR pathway is also targeted by Tavneos (avacopan), an oral AAV therapy taken twice daily. Tavneos selectively binds to C5aR, preventing its interaction with C5a. However, concerns about the reliability and handling of data from its pivotal clinical trial led the FDA’s Center for Drug Evaluation and Research to propose withdrawing Tavneos’ U.S. approval, while a European Medicines Agency committee recommended revoking its marketing authorization in the European Union.
Mirador said there remains a need for next-generation therapies that provide durable suppression of the complement pathway while maintaining a favorable safety and tolerability profile. The company believes KP-301, an experimental injectable therapy, is well positioned to help address that need.
KP-301 uses a long-acting ‘sweeping’ mechanism
KP-301 takes a different approach by binding to the C5a protein itself before it can activate immune cells. According to Mirador, KP-301 is engineered as a long-acting, potent and selective antibody that uses pH-dependent target binding and antibody recycling.
This “sweeping” mechanism is intended to keep C5a suppressed for longer periods, allowing low, infrequent dosing that may be suitable for long-term treatment of chronic complement-mediated diseases such as AAV.
“The addition of KP-301 is enabled by the same disciplined, precision-driven approach that guides Mirador’s broader pipeline,” the release stated. The company’s Mirador360 precision development engine uses more than 2.5 million molecular profiles from immune-mediated diseases to support drug target validation, patient selection, and decisions about which diseases to prioritize for clinical development.
“Our strategy is disciplined: We take on big problems in [immunology and inflammation] and pair each program with the modality most likely to succeed for patients,” McKenna said. “KP-301 is a textbook example of that thesis.”
Under the agreement, Kira Pharmaceuticals will receive $12 million upon signing and may receive additional development and sales milestone payments.
Mirador also intends to evaluate KP-301 alone and in combination with other medicines, with the goal of expanding its development into additional inflammatory diseases.
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