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Colivelin (TFA) is a neuroprotective peptide and activator of STAT3. STAT3 Amyloid-β

Colivelin (TFA) is a hybrid peptide composed of ADNF and AGA-(C8R)HNG17, a potent Humanin (HN) derivative[2]. Humanin (HN) and its derivatives, such as Colivelin (TFA), suppress neuronal death induced by insults related to Alzheimer's disease (AD) by activating STAT3[1]. Colivelin (TFA) completely suppresses death induced by overexpressed FAD-causative genes and A 1-43 at a concentration of 100 fM, whereas AGA-(C8R)HNG17 does so at a concentration of 10 pM[2].

Humanin (HN) and its derivatives, such as Colivelin (TFA) also ameliorate functional memory impairment of mice induced by anticholinergic drugs or soluble toxic amyloid-β (Aβ)[1]. Intracerebroventricular administration of Colivelin (TFA) not only completely suppresses impairment in spatial working memory induced by repetitive intracerebroventricular injection of Aβ25-35 or Aβ1-42, but also it antagonizes neuronal loss in the CA1 region of hippocampus induced by hippocampal injection of Aβ1-42[2].

[1]. Yamada M, et al. Nasal Colivelin treatment ameliorates memory impairment related to Alzheimer's disease. Neuropsychopharmacology. 2008 Jul;33(8):2020-32. [2]. Chiba T, et al. Development of a femtomolar-acting humanin derivative named colivelin by attaching activity-dependent neurotrophic factor to its N terminus: characterization of colivelin-mediated neuroprotection against Alzheimer's disease-relevant insults in vitro and in vivo. J Neurosci. 2005 Nov 2;25(44):10252-61.

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