On December 14, 2015 Cyclacel Pharmaceuticals, Inc. (Nasdaq:CYCC) (Nasdaq:CYCCP) ("Cyclacel" or the "Company"), reported the presentation of preclinical data demonstrating the molecular basis for the development of CYC065 in triple negative breast cancer (TNBC), and in particular basal-like TNBC. CYC065 is a highly-selective, second-generation cyclin dependent kinase (CDK) inhibitor targeting CDK2/9 dependent tumors (Press release, Cyclacel, DEC 14, 2015, View Source [SID:1234508697]). The data were presented at the San Antonio Breast Cancer Symposium (SABCS), taking place December 8-12, 2015.

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"We have recently reported that CYC065 can target malignancies driven by CDK2/9 dependent oncogenic and leukemogenic pathways such as MLL-rearranged leukemias and tumors overexpressing MYC", said Spiro Rombotis, Cyclacel’s President and Chief Executive Officer. "The data presented at SABCS show CYC065 could be active in breast cancer patients with a poor prognosis and that its mechanism induces breast cancer cell death by apoptosis. In addition, we have identified approved and investigational anticancer agents, including our own sapacitabine, which combine effectively with CYC065. A first-in-human, Phase 1 clinical trial with CYC065 has commenced and we look forward to reporting data from this study."

Data presented at SABCS (Program Number: P5-03-10, View Source) demonstrated in particular the mechanistic rationale for clinical development of CYC065 in basal-like TNBC, a cancer with poor prognosis frequently associated with BRCA1 mutations. Molecular characteristics of TNBC include amplification or overexpression of Cyclin E, the partner protein of CDK2, and MYC. CYC065 directs a pro-apoptotic mechanism in breast cancer cell lines, which includes transcriptional down regulation of key pro-survival and oncogenic regulators, including MCL-1 and MYC.

CYC065 was shown to rapidly induce cell death in breast cancer cell lines, while transiently inducing G1 cell cycle arrest in non-malignant breast lines. CYC065’s potent anticancer activity has been confirmed in breast cancer xenograft animal models. CYC065 effectively combined with Cyclacel’s sapacitabine in breast cancer cell lines, as was the case with seliciclib, Cyclacel’s first generation CDK2/9 inhibitor, when combined with sapacitabine.

An oral regimen of seliciclib and sapacitabine is being evaluated in an on-going Phase 1 all-comer study of patients with various advanced cancers. In previously reported initial data from this study, durable partial responses have been observed in breast, ovarian and pancreatic cancer patients with germline mutations in Homologous Recombination (HR) repair genes, specifically BRCA1 or BRCA2.

CYC065 is in a first-in-human, Phase 1 clinical trial.