BiPER Therapeutics’ lead program is a first-in-class small molecule targeting GRP78/ BiP. Tumors thrive under adverse conditions, such as hypoxia, nutrient starvation, and oxidative stress, by adjusting their protein-folding capacity via overexpression of GRP78. Overexpression of GRP78 is associated with very poor prognosis of patients in a broad range of cancer indications.
BPR001 has a unique, selective mechanism-of-action that selectively kills cancerous cells. BPR001 induces strong and lethal ER Stress through selective GRP78 binding and inhibition, leading to cancer cellular death via apoptosis and autophagy. As cancer cells express permanent and high ER Stress level to survive, proliferate and become resistant to standard of care therapies – by targeting this pathway, BPR001 is able to overcome this survival mechanism and this resistance, improving outcomes in both sensitive and resistant cancers.
Large body of in vivo and in vitro efficacy and tolerability data support the proof-of-concept for BPR001 use as an oral anti-cancer therapy. BPR001 has demonstrated efficacy in a broad range of cancer indications in monotherapy and in combination associated with an excellent pharmacological and tolerability profile. BPR001 activates also immune response, as demonstrated by production of interferon gamma and significant tumor reduction, and activation of immune cell death.
Most current treatment strategies for advanced cancers are either effective in only some patient populations or have high relapse rates. BPR001 is designed to be used in monotherapy or in combination with these treatments to improve patient outcomes. In preclinical studies, patent-protected data demonstrate that BPR001 is effective in monotherapy and enhances a wide range of therapies, including standard of care agents like chemotherapies, targeted therapies and immunotherapies.
BPR002 is a first-in-class small molecule series inducing ER Stress associated with strong immunomodulation properties. BPR002 leads series are first-in-class ER stress inducers being selected on their immune-cell mediated cancer-cell killing properties.
Our BPR002 series shown preliminary immunomodulation properties which is consistent with recent studies that have uncovered a mechanism by which controlled ER Stress promotes malignant progression: by subverting the protective function of innate immune cells in the tumor microenvironment to cripple the development of anti-tumor immunity. Our strategy for BPR002 is to select candidates able to harness the intrinsic ability of immune system to recognize and eliminate malignant cells through ER Stress modulation.
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