Calibr and Bill & Melinda Gates Medical Research Institute announce licensing agreement for novel candidate tuberculosis treatment compound

Calibr, a division of Scripps Research dedicated to the “bench to bedside” development of transformative medicines, and the Bill & Melinda Gates Medical Research Institute  announced a strategic licensing agreement to advance development of a novel investigational compound for tuberculosis treatment. Under the agreement, Calibr is granting Gates MRI an exclusive license to continue the development of the investigational compound CLB073 for tuberculosis treatment. Calibr will transition CLB073 to Gates MRI for further development.

“Eradicating tuberculosis will require enhancing the world’s current therapeutic options—meaning shortening treatment duration and overcoming drug resistance,” says Case McNamara, PhD, senior director of Infectious Disease at Calibr. “At Calibr, we have been working with collaborators, through the support of the Bill & Melinda Gates Foundation, to discover and develop novel medicines for diseases that require improved treatment regimens, such as tuberculosis. We hope our collaboration with Gates MRI to advance CLB073 will ultimately be able to help the millions of people who contract this deadly disease.”

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Tuberculosis is a severe disease caused by the bacterium Mycobacterium tuberculosis (Mtb). Mtb is known to sequester in lung macrophages following infection. Macrophages are a type of immune defense cell that typically kill infecting microorganisms. Mtb has the ability to establish a prolonged infection in these cells and, under certain conditions, relies on the macrophage’s cholesterol supply as a key carbon source for growth.

To develop a drug capable of targeting Mtb in a new way, scientists at Calibr collaborated with researchers at the Cornell University College of Veterinary Medicine, including David Russell, PhD, the William Kaplan Professor of Infection Biology, and Brian VanderVen, PhD, an associate professor of Microbiology & Immunology. Together, they discovered and pre-clinically studied CLB073, which uses a novel mechanism to weaken Mtb’s intramacrophage survival.

SOURCE: PR Newswire

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