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Key Phase 1 Inclusion Criteria. 1. ECOG Performance Status of 0-1. 2. Measurable disease. 3. Willing to undergo a tumor biopsy. 4. Histologically-proven B cell malignancies, meeting the following criteria: 1. Relapsed, refractory B-cell non-Hodgkin lymphoma requiring therapy. 2. Relapsed, refractory chronic lymphocytic leukemia requiring therapy. 3. Relapsed or progressive multiple myeloma on or after treatment. 5. Histologically-proven solid tumor meeting the following criteria: 1. Metastatic breast cancer. 2. Recurrent squamous cell carcinoma of the head and neck. 3. Ovarian cancer. 4. Soft tissue sarcoma. 5. Recurrent metastatic or locally advanced pancreatic cancer. 6. Advanced small-cell lung cancer. Key Phase 2 Inclusion Criteria. 1. ECOG Performance Status of 0-1. 2. Measurable disease defined by disease-specific response criteria. 3. Site of disease amenable to a biopsy and willing to undergo a biopsy. 4. Biomarker positive on recent biopsy or bone marrow sample if required. 5. Histologically-proven B cell malignancies, meeting the following criteria: DLBCL, MCL, or Multiple Myeloma requiring therapy. 6. Histologically-proven solid tumors: 1. Triple negative breast cancer. 2. Ovarian cancer. 3. Pancreatic cancer. 4. Soft tissue sarcoma. 5. Other biomarker positive cancers. Key Exclusion Criteria. 1. Known active brain metastases. 2. Known history of meningeal involvement or meningeal carcinomatosis. 3. Spinal cord compression not definitively treated with surgery and/or radiation. 4. Laboratory assessments. 1. ANC < 1.0 x 10^9/L; PLT < 75 x 10^9/L; Hgb < 9.0 g/dL. 2. Calculated Creatinine clearance (Cockcroft-Gault) < 40 mL/min. 3. Hepatic function: AST > 2.0 x ULN; ALT > 2.0 x ULN; 4. Total bilirubin > 1.5 x ULN; 5. Albumin < 2.8 g/dL. 5. Screening QTc interval > 450 milliseconds (males) and > 470 ms for females

Overexpression of activation-induced cytidine deaminase (AID) or other cytidine deaminases causes high rates of deoxyribonucleic acid (DNA) damage (mutations, double strand DNA breaks, and chromosome rearrangements) in a high number of patients with B-cell malignancies, such as NHL, MM, and CLL, and in a subset of patients with solid tumors, such as non-small cell lung cancer (NSCLC), sarcoma, breast cancer, ovarian cancer, and squamous cell carcinoma of the head and neck. Cancer cells that overexpress AID and other cytidine deaminases rely on RAD51, a protein involved in homologous recombination, to repair the DNA damage caused by cytidine deaminases. Inhibition of RAD51 with CYT-0851 in preclinical models induces cell death, tumor growth delay or tumor regression. The Phase 1 part of the study will follow an accelerated titration design, which includes enrollment of single patient cohorts until certain criteria are met, followed by a standard 3+3 design. This design will allow for identification of a recommended phase 2 dose (RP2D) level while dosing the least number of patients as possible at potentially sub-therapeutic doses. In the Phase 2 part of the study, preliminary efficacy will be evaluated in 8 expansion cohorts (total n = 92-220), using a Simon two-stage design. The RP2D will be selected based on the MTD, the safety profile, PK, and available pharmacodynamics data generated from all subjects in Phase 1. In both Phase 1 and Phase 2, patients will be treated in continuous 28-day cycles and all patients will be assessed for response every 2 cycles. Treatment will be terminated if the patient progresses, cannot tolerate treatment, or withdraws consent from active therapy. Patients will undergo a safety evaluation approximately 1 month (28-35 days) after the last dose. Patients will be followed for response until progression is documented.

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