PROJECTS

SPR113 TUBERCULOSIS

SPR113 an IND candidate for drug-resistant and drug-sensitive tuberculosis

SPR113 is a lead small molecule under advance preclinical evaluation (IND enabling studies) with the potential to treat MDR/XDR and TDR form of tuberculosis. This molecule has the potential to restrict the growth of all drug resistant forms of Mycobacterium tuberculosis, and is under Investigational New Drug (IND) enabling studies in collaboration with a private pharmaceutical company. On successful completion of IND enabling studies, an IND with USFDA will be filed for phase 1 human clinical trial.

HIV-1 INFECTION

A lead molecule that employs a novel mode of action against HIV-1 infection

DDRC has developed a lead molecule that displays potent activity against HIV-1 infection in cells. Importantly, this lead molecule employs a novel mode of action that combines direct anti-viral activity with stimulation of a key innate defense response of the host cell. Our current emphasis is to validate and optimize this lead molecule further to develop an IND candidate, followed by IND enabling studies.

Cardiac Hypertrophy

A lead candidate with activity against cardiac hypertrophy

DDRC has developed a lead molecule that can significantly protect against cardiac hypertrophy and cardiomyocyte death. Proof-of-concept has also been demonstrated in the rat model where significant reduction in markers of cardiac hypertrophy was noted, along with a marked inhibition of cardiomycoyte apoptosis. These effects were also accompanied by a pronounced improvement in cardiac function. Importantly, this lead molecule employs a novel mechanism of action that has not been exploited so far. We are now in the process of optimizing this lead towards an IND candidate, followed by IND enabling studies.

NON-Alcoholic Fatty Liver Disease

Exploiting autophagy as a novel treatment strategy for Non-alcoholic Fatty Liver Disease (NAFLD)

Using our in-house developed library of small molecules that stimulate cellular autophagy through a novel mechanism, we have identified a hit that suppresses lipid accumulation in hepatocytes. A ‘hit-to-lead’ optimization process is currently underway, with the eventual goal of arriving at an IND candidate for subsequent development.