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Cellerant Therapeutics, Inc. Awarded $6.86 Million Grant From California Institute for Regenerative Medicine to Support Development of Novel Antibody-Drug Conjugate for AML

Cellerant Therapeutics,Inc.
Posted on: 22 Aug 17

Cellerant Therapeutics, Inc., a clinical-stage company developing innovative immunotherapies for hematologic malignancies and other blood-related disorders, today announced it has been awarded a grant from the California Institute for Regenerative Medicine (CIRM) for up to $6.86 million to support preclinical development and the filing of an Investigational New Drug application (IND) for CLT030-ADC, Cellerant’s antibody-drug conjugate (ADC) product for the treatment for acute myeloid leukemia (AML). AML is an aggressive cancer with high relapse rates and low overall survival, which are thought to be due to the persistence of leukemic stem cells that are relatively resistant to current chemotherapy regimens. CLT030-ADC targets C-type-like lectin 1 (CLL1), a cell surface antigen highly expressed on leukemic stem cells but not on normal hematopoietic stem and progenitor cells.

CIRM is an agency of the State of California whose mission is to accelerate stem cell treatments to patients with unmet medical needs. CIRM grants are awarded through a competitive process which includes rigorous review and evaluation by independent scientific and medical experts.

"We are honored to receive this award from CIRM, which will help us advance the development of CLT030-ADC,” said Ram Mandalam, Ph.D., President and Chief Executive Officer of Cellerant. “Based on target characteristics and preclinical results, CLT030-ADC has the potential to increase survival and become a first-in-class treatment for AML patients. We are excited to be working with CIRM to develop this novel therapeutic for an unmet medical need.”

“Our mission here at CIRM is to support novel stem cell-based therapeutics, including those that target cancer stem cells,” added Maria Millan, M.D., interim President and CEO of CIRM. “Cancer stem cells are believed to play a key role in tumor formation and growth, so attacking them has the potential to improve patient outcomes in deadly diseases such as AML.”

CLT030-ADC consists of an antibody targeting CLL1 linked to a DNA-damaging cytotoxic payload. CLL1 is an antigen expressed specifically on AML cancer stem cells and not on normal hematopoietic stem cells. The Company and others have shown that CLL1 is expressed in approximately 90% of all AML patient types, including all French American British classifications, all cytogenetic risk categories, and in patients independent of FLT-3 status. In preclinical AML models, CLT030-ADC demonstrated complete target-dependent tumor regression. Importantly, CLT030-ADC should have minimal effect on the formation of

normal blood cell types because CLL1 is not expressed on normal hematopoietic stem cells and minimally on progenitor cells. This would potentially be an important safety advantage compared to other targeted therapies for AML where the target antigen is expressed on normal stem and progenitor cells, such as CD33.

About Cellerant Therapeutics

Cellerant Therapeutics is a clinical-stage company developing innovative cell- and antibody-based immunotherapies for hematologic malignancies and other blood-related disorders. Cellerant’s CLT-008 (human myeloid progenitor cells) is a universal cell therapy for the treatment of neutropenia. Chemotherapy-induced neutropenia is a severe side effect of many chemotherapy regimens, particularly for AML and other hematologic malignancies. CLT-008 is currently in a randomized, controlled Phase 2 clinical trial in patients with AML. Cellerant’s is developing two antibody drug-conjugate (ADC) product candidates: CLT030-ADC, intended to treat AML by selectively targeting and killing leukemic stem and blast cells, and CLT012-ADC, which could be a potential treatment for AML and a number of solid tumors. For more information, visit: www.cellerant.com

View source version on businesswire.com: http://www.businesswire.com/news/home/20170822005387/en/

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Last updated on: 22/08/2017

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