We are applying our RIPTAC therapeutics to build a robust pipeline of new precision treatments for many cancers. The hold and kill mechanism has the potential to overcome current by-pass resistance, a stubborn and, unfortunately, common problem with today’s precision oncology therapies. Our initial focus will be on bringing new therapeutics to address these difficult-to-treat patient populations.

Our most advanced drug programs are for common solid tumors types to address the unmet treatment needs of drug resistant patients. Our lead drug candidate is a RIPTAC therapeutic for the treatment of metastatic, castrate resistant prostate cancer. Halda’s pipeline includes additional RIPTAC pipeline programs in development across a range of cancers, including treatment of earlier stages of cancer.

Lead Drug Program for Prostate Cancer – RIPTAC Therapeutic leveraging Androgen Receptor targeting

Our lead drug candidate is an orally-available RIPTAC therapeutic with a novel mechanism designed to overcome resistance in the treatment of metastatic, castration resistant prostate cancer (mCRPC), followed by earlier lines of therapy. Halda has presented preclinical data showing its heterobifunctional hold and kill mechanism that utilizes androgen receptor (AR) as a targeting protein to selectively deliver the RIPTAC to tumors and an essential protein involved in transcriptional regulation. The ensuing trimeric complex results in the abrogation of the essential protein function and selective prostate cancer cell death. We have demonstrated in vivo activity in rodent models of prostate cancer and in vitro activity across widely used prostate cancer cell lines.

The unmet need in metastatic, castration resistant prostate cancer (mCRPC):

In the U.S., 1 in 8 men will be diagnosed with prostate cancer in his lifetime. Initially Prostate cancer depends on the androgen receptor (AR), a transcriptional factor critical for prostate cancer growth and progression. Treatment initially relies on androgen deprivation therapy, as well as AR signaling inhibitors (ARSIs).  However, resistance to antiandrogen interventions eventually emerges, and is driven by many heterogenous bypass mechanisms including genomic alterations in AR. In the metastatic, castration resistance form of the disease, AR remains expressed in tumors that are no longer AR dependent and in fact is amplified in many late stage patients, and thus serves as a suitable targeting protein for prostate cancer RIPTAC therapeutics to address a vast unmet need.

See the details of Halda’s data presentation at ASCO GU Symposium (February 2023)

for this novel oral RIPTAC therapeutic for prostate cancer

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