Pipeline ++ Our Pipeline

Pipeline ++ Our Programs

BTX-1188 (GSPT1 + IKZF1/3)

BTX-1188, our lead product candidate, is a rationally designed dual-targeting molecular glue degrader of GSPT1 and IKZF1/3 that we are developing for the treatment of hematologic malignancies and solid tumors. We believe that the combination of degrading GSPT1, a promising oncology target, and IKZF1/3, clinically validated immunomodulatory targets, provides advantages relative to GSPT1-only degradation. We are currently enrolling patients in a Phase 1/2 clinical trial of BTX-1188 with preliminary results expected in late 2022/early 2023.

Pipeline ++ Our Programs

BTX-1188 (GSPT1 + IKZF1/3)

BTX-1188, our lead product candidate, is a rationally designed dual-targeting molecular glue degrader of GSPT1 and IKZF1/3 that we are developing for the treatment of hematologic malignancies and solid tumors. We believe that the combination of degrading GSPT1, a promising oncology target, and IKZF1/3, clinically validated immunomodulatory targets, provides advantages relative to GSPT1-only degradation. We are currently enrolling patients in a Phase 1/2 clinical trial of BTX-1188 with preliminary results expected in late 2022/early 2023.

Pipeline ++ Our Programs

Undisclosed Glue Discovery

We have a broad discovery program leveraging parallel in silico and in vitro approaches to identify novel neosubstrates that could be degraded by Cereblon-based molecular glues. This effort has already identified several potential new targets previously considered undruggable and with relevance across a range of cancers. We look forward to translating these efforts into novel molecular glue programs in the future.

Pipeline ++ Our Programs

Undisclosed Glue Discovery

We have a broad discovery program leveraging parallel in silico and in vitro approaches to identify novel neosubstrates that could be degraded by Cereblon-based molecular glues. This effort has already identified several potential new targets previously considered undruggable and with relevance across a range of cancers. We look forward to translating these efforts into novel molecular glue programs in the future.

Pipeline ++ Our Programs

SOS1

We are developing degraders of Son of Sevenless 1 (SOS1), an important upstream target in the Kirsten rat sarcoma virus (KRAS) pathway. We are also in early stages of discovery in developing degraders directly targeting KRAS. KRAS is the most frequently mutated cancer-causing oncogene and is mutated in over 20% of all human cancers, including an estimated 90% of pancreatic tumors, 45% of colorectal tumors, and 30% of lung tumors. In preclinical models, we have demonstrated that our lead candidates rapidly and potently degraded SOS1 by up to 90% with inhibition of pan-KRAS mutant cancer cell lines. We anticipate selecting a development candidate from this program and initiating IND-enabling studies in 2023.

Pipeline ++ Our Programs

SOS1

We are developing degraders of Son of Sevenless 1 (SOS1), an important upstream target in the Kirsten rat sarcoma virus (KRAS) pathway. We are also in early stages of discovery in developing degraders directly targeting KRAS. KRAS is the most frequently mutated cancer-causing oncogene and is mutated in over 20% of all human cancers, including an estimated 90% of pancreatic tumors, 45% of colorectal tumors, and 30% of lung tumors. In preclinical models, we have demonstrated that our lead candidates rapidly and potently degraded SOS1 by up to 90% with inhibition of pan-KRAS mutant cancer cell lines. We anticipate selecting a development candidate from this program and initiating IND-enabling studies in 2023.

Pipeline ++ Our Programs

CDK2/4/6

We are developing degraders of cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6), important targets for a range of cancers including 30% of breast and esophageal cancers, 50% of pancreatic and 40% of bladder cancers. CDK4 and CDK6 are clinically validated targets in the context of breast cancers. In preclinical breast cancer models, our lead candidates potently degrade CDK4 and CDK6 resulting in robust inhibition of phosphorylated Rb and cell cycle arrest. We anticipate selecting a development candidate from this program and initiating IND-enabling studies in 2023.

Pipeline ++ Our Programs

CDK2/4/6

We are developing degraders of cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6), important targets for a range of cancers including 30% of breast and esophageal cancers, 50% of pancreatic and 40% of bladder cancers. CDK4 and CDK6 are clinically validated targets in the context of breast cancers. In preclinical breast cancer models, our lead candidates potently degrade CDK4 and CDK6 resulting in robust inhibition of phosphorylated Rb and cell cycle arrest. We anticipate selecting a development candidate from this program and initiating IND-enabling studies in 2023.

PDE4 program

We are developing degraders of Phosphodiesterase 4 (PDE4), a validated target for auto-immune and inflammatory diseases such as psoriasis. Our first-in-class degraders are highly selective for PDE4 degradation and have shown greater potency than PDE4 inhibitors in terms of inhibition of key cytokines such as TNF-α, IFN-γand IL-1β in preclinical models. We anticipate selecting a development candidate from this program and initiating IND-enabling studies in 2023.

PDE4 program

We are developing degraders of Phosphodiesterase 4 (PDE4), a validated target for auto-immune and inflammatory diseases such as psoriasis. Our first-in-class degraders are highly selective for PDE4 degradation and have shown greater potency than PDE4 inhibitors in terms of inhibition of key cytokines such as TNF-α, IFN-γand IL-1β in preclinical models. We anticipate selecting a development candidate from this program and initiating IND-enabling studies in 2023.

*Full pipeline is wholly owned by Biotheryx.

Pipeline ++ Partner With Us

We are seeking collaboration opportunities that can broaden and accelerate the impact of our platform and programs. Contact us at [email protected].