Pioneering a New Cancer Treatment Paradigm

Treatment resistance, cancer relapse and metastasis are too often the unfortunate outcome for cancer patients. We have evidence that a common feature of tumors that resist treatment, relapse, and metastasize is the induction of adaptive stress. We are pioneering the development of differentiated treatment approaches that are designed to target mechanisms that arise as a result of adaptive stress induction to help enable patients to live longer, cancer free lives.

Pioneering a New Cancer Treatment Paradigm

Treatment resistance, cancer relapse and metastasis are too often the unfortunate outcome for cancer patients. We have evidence that a common feature of tumors that resist treatment, relapse, and metastasize is the induction of adaptive stress. We are pioneering the development of differentiated treatment approaches that are designed to target mechanisms that arise as a result of adaptive stress induction to help enable patients to live longer, cancer free lives.

Pioneering a New Cancer Treatment Paradigm

Treatment resistance, cancer relapse and metastasis are too often the unfortunate outcome for cancer patients. We have evidence that a common feature of tumors that resist treatment, relapse, and metastasize is the induction of adaptive stress. We are pioneering the development of differentiated treatment approaches that are designed to target mechanisms that arise as a result of adaptive stress induction to help enable patients to live longer, cancer free lives.

Working to Exploit Stress Driven Vulnerabilities in Cancer Cells

Despite clinical improvements made with the use of approved precision therapies and therapeutic candidates, cancer cells leverage adaptive stress-mitigating pathways and immunosuppression to adapt, survive, and become resistant to treatment. However, stress also causes cells to be more vulnerable to alternative therapeutic approaches. We believe that we can work to exploit these vulnerabilities through the following approaches:

  1. Inhibit stress-mitigating pathways (HC-5404): Prevent cancer cell survival and adaptation by inhibiting stress-mitigation pathways
  2. Increase stress signaling (HC-7366): Overwhelm stress-mitigation pathways and induce apoptosis (cell death) by hyperactivation
  3. Exploit stress-induced vulnerabilities (odetiglucan): Target tumor-immune interactions to exploit stress-induced, ecosystem vulnerabilities in the tumor microenvironment

Our Clinical-Stage Therapeutic Candidates

HC-7366

 

HC-7366 is our differentiated, first-in-human therapeutic candidate designed to activate the General Control Nonderepressible 2 (GCN2) kinase. GCN2 is critical to the function of the Integrated Stress Response (ISR) signaling pathway.

HC-5404

 

HC-5404 is our differentiated, first-in-human therapeutic candidate designed to inhibit PKR-like Endoplasmic Reticulum Kinase (PERK). PERK is critical to the function of the Unfolded Protein Response (UPR) signaling pathway.

Odetiglucan

 

Odetiglucan is a differentiated, systemically administered therapeutic candidate that has been observed preclinically to play an important role in tumor immune interactions by modulating both the innate and adaptive immune system.

In preclinical studies and clinical testing, it has been shown to have the potential to bind to a unique combination of receptors on innate immune cells, reprogramming the tumor microenvironment to drive a strong anti-cancer immune response.

Proven Leadership Team

Our team is led by proven biotech executives who believe combining traditional drug development methods with computational expertise will enable efficient clinical development of our first-in-human therapeutic candidates. Our team embodies the values of scientific rigor and urgency, which are important to our mission of developing therapeutics that improve the lives of patients.