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.
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 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.
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[1]
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:
Significantly 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/0.21mL; 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].
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
2759.12
Formula
C119H206N32O35.C2HF3O2
Sequence Shortening
SALLRSIPAPAGASRLLLLTGEIDLP
运输条件
Room temperature in continental US; may vary elsewhere.
请依序添加每种溶剂：;Water with 5% sefsol and 20% isopropanol
Solubility: 6.25 mg/mL (2.27 mM); Suspended solution; Need ultrasonic
*以上所有助溶剂都可在 MCE 网站选购。
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]. Zhao H, et al. Colivelin Rescues Ischemic Neuron and Axons Involving JAK/STAT3 Signaling Pathway.Neuroscience. 2019 Sep 15;416:198-206.
[3]. 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.
[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.
