A compound with these five characteristics would be a major advance in the treatment of cancer.
CT-262 is a prodrug delivery system that selectively releases a highly cytotoxic moiety intracellularly in cancer cells, sparing healthy cells.
Active moiety is an analogue of duocarmycin with highly potent antitumor activity
Novel design – nothing like it examined previously - creates potential for major advance in the treatment of cancer
Prodrug is inactive and highly stable in plasma, greatly limiting the potential for off-target toxicity
Selective intracellular release in cancer cells of toxic duocarmycin moiety – free drug - from prodrug driven by protein in cytosol of cancer cells that does not appear to be meaningfully present in healthy cells
Targeting of cancer cells not dependent upon presence of cell surface antigen – all cancer cells targeted
CT-262 highly efficacious in in vivo xenograft and transgenic cancer models, as well as in organoid models highly predictive of efficacy in humans
Low toxicity, low myelosuppression that typically limits chemotherapy
Not subject to traditional mechanisms of resistance (unable to raise resistance to date)
Combination of results from preclinical efficacy studies and safety evaluations demonstrate CT-262 is highly efficacious and broadly active, and suggests the compound has a wide therapeutic window.
CT-262 is a Prodrug That is Selectively Activated in Cancer Cells and Targets DNA to Induce Programmed Cell Death
CT-262 is an analogue of duocarmycin, a natural product with potent anti-tumor activity.
CT-262 Undergoes a Two-Step Process for Selective Activation Inside Cancer Cells Delivering Primed Drugs Selectively to Cancer Cells
Contrast With Traditional Chemotherapy – Potential for Wide Therapeutic Window
Selective Activation Shown in Mice with Breast Cancer: Inactive Prodrug is Converted to Primed Drug in Breast Cancer Tissue but Not in Normal Breast Tissue
Highly Potent & Broadly Active in a Range of Human Cancers
Data demonstrate CT-262 is readily converted from inactive form to cytotoxic form in human cancers.
CT-262 Shows Pronounced Activity Against Highly Resistant Human NSCLC in Murine Xenograft Model
CT-262 inhibits tumor growth in a dose-dependent manner and continues inhibition after the last dose.
CT-262 is Highly Potent, Efficacious and Broadly Active in Organoid Models of Cancer that are Predictive of Human Efficacy
Data demonstrate CT-262 is readily converted from inactive form to cytotoxic form in human cancers.
CT-262 Should Be Much Less Susceptible to Cancer Cell Resistance Mechanisms Than Leading Therapies