Carrick Therapeutics Announces $35 Million Investment from Pfizer
Funding supports advancement of samuraciclib, an oral CDK7 inhibitor, in combination with endocrine therapy for HR+, HER2- advanced breast cancer
Adam Schayowitz, Ph.D., Vice President and Development Head, Breast Cancer, Colorectal Cancer and Melanoma, Pfizer Global Product Development, joins Scientific Advisory Board
DUBLIN, Ireland and BOSTON, Dec. 01, 2022 (GLOBE NEWSWIRE) -- Carrick Therapeutics, an oncology-focused biopharmaceutical company discovering and developing highly differentiated therapies, today announced a $35 million investment from Pfizer to support its rapid development of samuraciclib (CT-7001) in HR+, HER2- breast cancer, which represents more than two thirds of all new female breast cancer cases.1
Carrick and Pfizer have also entered into an agreement under which Pfizer will provide global development capabilities and expertise to support Carrick’s Phase 2 study of samuraciclib in combination with fulvestrant for CDK4/6i-resistant HR+, HER2- advanced breast cancer. Carrick will maintain full economic ownership and control of samuraciclib and its pipeline. In conjunction with the investment, Adam Schayowitz, Ph.D., Vice President and Development Head, Breast Cancer, Colorectal Cancer and Melanoma, Pfizer Global Product Development, will join Carrick’s Scientific Advisory Board.
“Given Pfizer’s deep expertise in developing treatments for breast cancer, we are delighted to welcome them as an investor and collaborator in developing samuraciclib,” said Tim Pearson, Chief Executive Officer of Carrick Therapeutics. “We believe Pfizer’s investment further underscores the potential of samuraciclib to be a first- and best-in-class treatment for patients with advanced breast cancer, following CDK4/6i therapy.”
“We believe samuraciclib has the potential to play a meaningful role in the treatment of HR+, HER2- breast cancer,” said Chris Boshoff, M.D., Ph.D., Chief Development Officer, Oncology & Rare Disease, Pfizer Global Product Development. “Our hope is that Pfizer’s development capabilities and expertise in breast cancer and next-generation cyclin dependent kinases, combined with the innovation represented by samuraciclib, will help accelerate the advancement of this potential breakthrough for patients.”
About Samuraciclib (CT7001)
Samuraciclib is the most advanced oral CDK7 inhibitor in clinical development. Inhibiting CDK7 is a promising therapeutic strategy in cancer, as CDK7 regulates transcription of cancer-causing genes and promotes uncontrolled cell cycle progression and resistance to anti-hormone therapy. Samuraciclib has demonstrated a favorable safety profile and encouraging efficacy in early clinical studies. In addition to the above studies, it is currently being evaluated in prostate cancer with further potential in pancreatic, ovarian and colorectal cancers. Samuraciclib has been granted Fast Track designation from the U.S. Food and Drug Administration (FDA) for use in combination with fulvestrant for the treatment of CDK4/6i-resistant HR+, HER2- advanced breast cancer. Carrick is also collaborating with Roche to evaluate a novel combination of samuraciclib and Roche’s oral SERD giredestrant in CDK4/6i-resistant HR+, HER2- metastatic breast cancer.
About Carrick Therapeutics
Carrick Therapeutics is an oncology-focused biopharmaceutical company leveraging its deep expertise to identify and develop highly differentiated novel therapies that address significant unmet needs. In addition to samuraciclib, Carrick is also developing a novel CDK12/13 inhibitor / Cyclin-K glue-degrader which has advanced into IND enabling toxicology studies.
For more information about Carrick Therapeutics, please visit www.carricktherapeutics.com.
Contact
Carrick Therapeutics
Jenny Horsfield, Chief Business Officer
jenny.horsfield@carricktherapeutics.com
Investors and Media
Kevin Lui, Real Chemistry
klui@realchemistry.com
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1 Female Breast Cancer Subtypes — Cancer Stat Facts. National Cancer Institute. https://seer.cancer.gov/statfacts/html/breast-subtypes.html. Accessed 18 October 2022.
Released December 1, 2022