MedChemExpress -Model COG1410 -878009-24-6

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COG1410 is an apolipoprotein E-derived peptide and an apoptosis inhibitor. COG1410 exerts neuroprotective and antiinflammatory effects in a murine model of traumatic brain injury (TBI). COG1410 can be used for the research of neurological disease[1][2].
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COG1410

MCE China:COG1410

Brand:MedChemExpress (MCE)

Cat. No.HY-P2136

CAS:878009-24-6

Purity:98.85%

Storage:Sealed storage, away from moisture and light, under nitrogen Powder -80°C 2 years -20°C 1 year *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light, under nitrogen)

Shipping:Room temperature in continental US; may vary elsewhere.

Description:COG1410 is an apolipoprotein E-derived peptide and an apoptosis inhibitor. COG1410 exerts neuroprotective and antiinflammatory effects in a murine model of traumatic brain injury (TBI). COG1410 can be used for the research of neurological disease.

In Vitro:COG1410 (1-25 μM; 48 h) decreases the production and release of NO and TNFα in BV2 microglia cells[1].

In Vivo:COG1410 (0.3-0.6 mg/kg; a single i.v.) exhibits significant improvement on a short term test of vestibulomotor function and on a long term test of spatial learning and memory in mice[1].?COG1410 (0.8 mg/kg; a single i.v.) improves vestibulomotor function, decreases poststroke locomotor asymmetry, and decreases infarct volume of the ipsilateral hemisphere in rats[2].

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References:

[1]. Laskowitz DT, et, al. COG1410, a novel apolipoprotein E-based peptide, improves functional recovery in a murine model of traumatic brain injury. J Neurotrauma. 2007 Jul;24(7):1093-107.  [Content Brief]

[2]. Tukhovskaya EA, et, al. COG1410, a novel apolipoprotein-E mimetic, improves functional and morphological recovery in a rat model of focal brain ischemia. J Neurosci Res. 2009 Feb 15;87(3):677-82.  [Content Brief]

[3]. Kuai L, et, al. Apolipoprotein E-Mimetic Peptide COG1410 Enhances Retinal Ganglion Cell Survival by Attenuating Inflammation and Apoptosis Following TONI. Front Neurosci. 2019 Sep 13;13:980.  [Content Brief]

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