IGC Pharma announces preclinical data on IGC-M3

IGC Pharma (IGC) announced preclinical data on its investigational molecule “IGC-M3”. The invitro results demonstrates that IGC-M3 may offer disease-modifying potential by targeting multiple biological mechanisms central to Alzheimer’s pathology, including amyloid aggregation, oxidative stress, mitochondrial dysfunction, and neuroinflammation. In biochemical and cellular models, IGC-M3: Inhibited aggregation of amyloid a central component in senile plaque formation; Promoted disassembly of pre-formed amyloid aggregates, thereby reducing the presence of toxic amyloid species; Neutralized reactive oxygen species and preserved mitochondrial membrane potential, Prevented programmed neuronal cell death by blocking cytochrome c release; And reduced pro-inflammatory signaling in activated microglial cells. The IGC-M3 molecule is a synthetic derivative featuring a tricyclic aromatic core containing a fused isoindolinone-imide structure. Attached to the nitrogen of the imide is a side chain consisting of a pyridine ring linked via a methylene group to a 1,2,3-triazole ring, a motif often associated with coordination potential and biological activity. Additionally, the molecule bears a benzyl substituent with a phenyl ring substituted by two hydroxyl groups in ortho and para positions, resembling a catechol moiety. This group may contribute polarity, antioxidant potential, and hydrogen bonding capacity. Compound IGC-M3 was synthesized with a yield of 81%, indicating a highly efficient route for the construction of this complex architecture. In SH-SY5Y human neuronal cells, IGC-M3 showed neuroprotective effects by preserving mitochondrial membrane potential and reducing the production of reactive oxygen species after Abeta42-induced damage. It also prevented the release of cytochrome c, an early marker of apoptosis, and significantly reduced programmed cell death. In BV2 microglial cells, which mediate neuroinflammatory responses in AD, IGC-M3 reduced Abeta42-induced activation, normalized mechanical cell parameters such as height, stiffness, and adhesion force, and decreased the expression of pro-inflammatory markers including NF-B and TNF-alpha, both associated with chronic inflammation in Alzheimer’s disease. Although these findings are limited to in vitro models, the breadth of biological effects observed suggests that M3 has the potential to modulate multiple pathways in the Alzheimer’s disease cascade. The Company expects that IGC-M3 will advance to in vivo studies to evaluate potential efficacy and safety in animal models. If benefits are confirmed, IGC-M3 could represent a promising candidate for the development of disease-modifying treatments aimed at slowing or halting neurodegenerative progression in Alzheimer’s disease. The development of innovative compounds like IGC-M3 offers renewed hope in the fight against Alzheimer’s, a disease that currently affects millions of individuals and families worldwide. Multifunctional molecules that can act on several pathological fronts at once may represent the next frontier in achieving meaningful clinical progress and improving patient outcomes.