IGC Pharma (NYSE: IGC) has announced preclinical findings on its investigational small molecule candidate for Alzheimer’s disease (AD) demonstrating 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.
According to IGC, in vitro assays showed that TGR-63 suppressed 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.
In a statement, Ram Mukunda, CEO of IGC, commented, “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. 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.”
