Apolipoprotein E fragment (133-149) – COG133

Apolipoprotein E (ApoE) mimetic peptide COG133 competes with the ApoE holoprotein for binding the low density lipoprotein (LDL) receptor. COG 133 mimetic peptide takes the incredible capabilities of acting the same way as the LDL receptor-binding domain of ApoE. Therefore, this peptide wields a non-competitive stance against the alpha-7 nicotinic acetylcholine receptor, which is not only implicated in long-term memory but also in neurotoxicity, stroke, myocardial infarction, sepsis, Alzheimer’s disease, cancer progression, and angiogenic/neurogenic activity. Moreover, COG133’s anti-apoptotic effects further accentuate its potential. By mimicking ApoE, COG 133 / ApoE(133-149) masterfully inhibits the NMDA receptor channel function through interactions with the low-density lipoprotein receptor-related protein. The peptide emerged as a potent agent in reducing inflammation, cellular infiltration, and demyelination, making strides in animal models of multiple sclerosis (MS) and the 5-fluorouracil model of intestinal mucositis. Indeed, COG-133 emerged as a champion to suppress symptoms of experimental autoimmune encephalomyelitis (EAE), curbing inflammation, demyelination, and cell infiltration in the spinal cord. ApoE (133-149) fragment additionally showcased its prowess by decreasing TNF-α and nitric oxide (NO) release in BV-2 microglia and counteracting LPS-induced increases in brain levels of TNF-α and IL-6 in mice. The peptide also stands as a guardian of hippocampal neuronal health and offers promise in delaying disease onset and reducing severity of EAE mouse model. COG133’s multifaceted influences on inflammation, cellular responses, and neuronal health open doors to novel therapies for neurological disorders. Its potential as a groundbreaking tool in understanding and combating MS holds the promise of improved treatments and enhanced quality of life for patients suffering from this particular disease.