1. JAK/STAT Signaling
    Stem Cell/Wnt
    Neuronal Signaling
  2. STAT
  3. Colivelin


目录号: HY-P1061

Colivelin 是一种具有大脑通透性的神经保护肽 (neuroprotective peptide),是 STAT3 的有效激活剂。Coliveli 通过激活 STAT3 在体外抑制神经元死亡。Colivelin 对神经毒性、Aβ 沉积,神经元细胞凋亡,在神经退行性疾病显示出长期有利的影响。Colivelin 具有潜力用于阿尔茨海默病和缺血性脑损伤治疗的相关研究。

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Custom Peptide Synthesis

Colivelin Chemical Structure

Colivelin Chemical Structure

CAS No. : 867021-83-8

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Colivelin is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro[1]. Colivelin exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease[2]. Colivelin has the potential for the treatment of alzheimer's disease and ischemic brain injury[1]

IC50 & Target[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, 4 hours) significantly increases the p-STAT3 protein levels in BV-2 cells[4].

Western Blot Analysis[4]

Cell Line: BV-2 cells.
Concentration: 50 µg/mL.
Incubation Time: 4 hours.
Result: Increased p-STAT3 levels.

Cell Viability Assay[5]

Cell Line: KYSE70 and TE8 cells.
Concentration: 0.5 μM.
Incubation Time: 1 hour (followed by CYT-Rx20 treatment)
Result: Sgnificantly suppressed the viability in KYSE70 and TE8 cells.
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/0.21 mL; 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[3].

Animal Model: CD-1 mice[1]
Dosage: 10 pmol/3 μl
Administration: Intracerebroventricular administration
Result: Completely suppressed Aβ 25-35-mediated impairment in spatial working memory and increased the number of immunoreactive neurons.
Animal Model: C57 mice[1]
Dosage: 1.4, 7, or 35 nM/0.21mL
Administration: Intraperitoneal administration
Result: Protected against cholinotoxin-induced amnesia in mice.
Animal Model: Male C57BL/6 mice[3]
Dosage: 1 mg/kg
Administration: Intraperitoneal administration
Result: Protected against ischemic brain injury, and improves neurological outcomes
Molecular Weight








Sequence Shortening



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ColivelinSTATAmyloid-ββ-amyloid peptideAbetaischemicbraininjuryneurologicalalzheimerdiseaseNeuroprotectantInhibitorinhibitorinhibit


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