IGC Pharma Reports TGR-63 Blocks Both Amyloid And Tau Aggregation In Alzheimer's; Advances Dual-Action Therapy Approach

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.

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.

These encouraging findings validate TGR-63's dual mechanism of action, which is protected under IGC Pharma's patent portfolio. Building on this foundation, the Company is well-positioned to advance TGR-63 through continued preclinical development with the goal of establishing a novel, disease-modifying approach to Alzheimer's that is distinct from current single-target therapies.