APTSTAT3-9R

APTSTAT3-9R;

APTSTAT3-9R 是一种特定的 STAT3 结合肽,通过特异性阻断 STAT3 磷酸化来抑制 STAT3 激活和下游信号传导。APTSTAT3-9R 具有抗增殖作用和抗肿瘤活性。

APTSTAT3-9Ramp;;

APTSTAT3-9R Chemical Structure

规格 是否有货
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生物活性

APTSTAT3-9R, a specific STAT3-binding peptide, inhibits STAT3 activation and downstream signaling by specifically blocking STAT3 phosphorylation. APTSTAT3-9R exerts antiproliferative effects and antitumor activity[1].

IC50 Target[1]

STAT3

;

体外研究
(In Vitro)

APTSTAT3-9R (7.5, 15, and 30 μmol/L; 6 hours) significantly reduces STAT3–DNA-binding activity in a dose-dependent manner in human lung carcinoma cells (A549)[1].
APTSTAT3-9R (30 μM; for 2 weeks) suppresses cell viability and proliferation of cancer cells and significantly suppresses colony formation. APTSTAT3-9R has IC50s of 10 to 20 μM in A549, B16F1 and HepG2 cells[1].
APTSTAT3-9R (7.5, 15, and 30 μmol/L; 6 hours) effectively inhibits phosphorylation of STAT3 but does not affect the level of AKT phosphorylation, indicating specificity of the aptide[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

APTSTAT3-9R (8 mg/kg in 50 μL; intratumorally injected every other day for a total of four injections) suppresses tumor growth in 6-week-old female BALB/c nude mice with A549 cells[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

4947.51

Formula

C223H330N80O51

Sequence

His-Gly-Phe-Gln-Trp-Pro-Gly-Ser-Trp-Thr-Trp-Glu-Asn-Gly-Lys-Trp-Thr-Trp-Lys-Gly-Ala-Tyr-Gln-Phe-Leu-Lys-Gly-Gly-Gly-Gly-Ser-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Arg

Sequence Shortening

HGFQWPGSWTWENGKWTWKGAYQFLKGGGGSRRRRRRRRR

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献
  • [1]. Daejin Kim, et al. A Specific STAT3-binding Peptide Exerts Antiproliferative Effects and Antitumor Activity by Inhibiting STAT3 Phosphorylation and Signaling. Cancer Res. 2014 Apr 15;74(8):2144-51.

Colivelin

Colivelin;

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的相关研究。

Colivelinamp;;

Colivelin Chemical Structure

CAS No. : 867021-83-8

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250 mg ; 询价 ;
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Colivelin 的其他形式现货产品:

Colivelin TFA

生物活性

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

STAT3

;

Amyloid-β

;

体外研究
(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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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.

体内研究
(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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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

分子量

2645.10

Formula

C119H206N32O35

CAS 号

867021-83-8

Sequence Shortening

SALLRSIPAPAGASRLLLLTGEIDLP

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献
  • [1]. 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.

    [2]. Pan Z, et al. Upregulation of HSP72 attenuates tendon adhesion by regulating fibroblast proliferation and collagen production via blockade of the STAT3 signaling pathway.Cell Signal. 2020 Mar 18:109606.

    [3]. Zhao H, et al. Colivelin Rescues Ischemic Neuron and Axons Involving JAK/STAT3 Signaling Pathway.Neuroscience. 2019 Sep 15;416:198-206.

    [4]. Fang YY, et al. MFG-E8 alleviates oxygen-glucose deprivation-induced neuronal cell apoptosis by STAT3 regulating the selective polarization of microglia. Int J Neurosci. 2020 Mar 12:1-10.

    [5]. Chiu WC, et al. The Synthetic β-Nitrostyrene Derivative CYT-Rx20 Inhibits Esophageal Tumor Growth and Metastasis via PI3K/AKT and STAT3 Pathways. PLoS One. 2016 Nov 22;11(11):e0166453.