Colivelin (TFA)

Colivelin TFA is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro^[1]. Colivelin TFA exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease^[2]. Colivelin TFA has the potential for the treatment of alzheimer's disease and ischemic brain injury^[1]. IC50 & Target:STAT3, Amyloid-β^[1] In Vitro: Colivelin completely suppresses death induced by overexpressed FAD-causative genes and Aβ1-43 at a concentration of 100 fm, and keep its neuroprotective action at or above the levels of 1 nm^[1].
Colivelin-induced neuroprotection occurs via two neuroprotective pathways: one mediated by Ca²⁺/calmodulin-dependent protein kinase IV, triggered by ADNF, and one mediated by signal transducer and activator of transcription 3, triggered by HN^[1].
Colivelin reverses caspase3, Bax and Bcl-2 expressions in HT22 cells medaited by rmMFG-E8 in the co-cultured cells under OGD condition^[4].
Colivelin (50 μg/mL, 24 hours) significantly increases the p-STAT3 protein levels in BV-2 cells^[4].
In Vivo: Colivelin(intracerebroventricular administration; 10 pmol/3 μl; 3 weeks) suppresses impairment in spatial working memory induced by repetitive intracerebroventricular injection of Aβ25-35 or Aβ1-42, in addition, it antagonizes neuronal loss in the CA1 region of hippocampus induced by hippocampal injection of Aβ1-42^[1].
Colivelin (intraperitoneal administration; 1.4, 7, or 35 nM/0.21mL; on the Y-maze testday) suppresses memory impairment caused by 3-quinuclidinyl benzilateand restricts functional memory deficit^[1].
Colivelin (intraperitoneal injection; 1 mg/kg; 14 days) results in improved motor and cognitive function with time by performance of mNSS, rotarod, and corner turning test.It also reduces lesion volume and improves neurological deficits after MCAO^[1].