IGC Pharma Releases Preclinical Data On TGR-63 Showing It Impacts Beta-Amyloid Pathology And Inhibits Tau Protein Aggregation Addressing Two Hallmarks Of Alzheimer's Disease

IGC Pharma, Inc. (NYSE:IGC) today announced preclinical findings on TGR-63, the Company's investigational small-molecule candidate for Alzheimer's disease. The data demonstrate that TGR-63 extends its therapeutic potential beyond previously reported effects on beta-amyloid (Aβ) pathology by also inhibiting tau protein aggregation, another key hallmark of Alzheimer's.

"These results underscore the potential of TGR-63 as a differentiated, dual-acting candidate that targets both beta-amyloid and tau, two central drivers of Alzheimer's pathology," said Ram Mukunda, CEO of IGC Pharma. "By broadening our portfolio with this important addition, we are strengthening IGC's capabilities in developing safer and more effective therapies that go beyond the limitations of current treatments. We are continuing to advance the preclinical evaluation of TGR-63 as we work toward building a pipeline of truly disease-modifying solutions for Alzheimer's."

In in vitro assays, TGR-63 was shown to suppress tau fibril formation at micromolar concentrations, suggesting its ability to interfere with the development of neurofibrillary tangles strongly associated with neuronal dysfunction and cognitive decline. This activity complements prior findings that TGR-63 effectively disrupts Aβ plaque aggregation.

Additionally, serum stability studies confirmed that TGR-63 retains its structural integrity under physiological conditions. The compound remained stable when incubated in phosphate-buffered saline (PBS) and mouse blood serum at 37 °C for several hours.

Complementary MALDI mass spectrometry further detected TGR-63 in serum samples at both 1- and 24-hours post-administration, supporting its pharmacological resilience and systemic delivery potential.