GsMTx4 TFA is a spider venom peptide that selectively inhibits cation-permeable mechanosensitive channels (MSCs) belonging to the Piezo and TRP channel families. GsMTx4 TFA is an important pharmacological tool for identifying the role of these excitatory MSCs in normal physiology and pathology[1]. GsMTx4 TFA significantly attenuates bladder hyperactivity[2].
IC50 Target
MSCs[1]
分子量
4215.91
Formula
C187H280N49F3O47S6
Sequence Shortening
GCLEFWWKCNPNDDKCCRPKLKCSKLFKLCNFSF
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Sealed storage, away from moisture and light
Powder
-80deg;C
2 years
-20deg;C
1 year
*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (sealed storage, away from moisture and light)
溶解性数据
In Vitro:;
DMSO : 10 mg/mL (2.37 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (ultrasonic) (insoluble)
配制储备液
浓度溶剂体积质量
1 mg
5 mg
10 mg
1 mM
0.2372 mL
1.1860 mL
2.3720 mL
5 mM
—
—
—
10 mM
—
—
—
*
请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
参考文献
[1]. Gnanasambandam R, et al. GsMTx4: Mechanism of Inhibiting Mechanosensitive Ion Channels. Biophys J. 2017 Jan 10;112(1):31-45.
[2]. Liu Q, et al. Increased Piezo1 channel activity in interstitial Cajal-like cells induces bladder hyperactivity by functionally interacting with NCX1 in rats with cyclophosphamide-induced cystitis. Exp Mol Med. 2018 May 7;50(5):60.
It is demonstrated that transarterial infusion of GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro integrin-inhibitor which includes RGD-peptide). As a synthetic linear RGD peptide, GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro) can inhibit the adherence of tumor cells to endothelial cells of blood vessels and limit its metastasis[1]. GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro) is used as a soluble integrin-blocking RGD-based peptide. GRGDSP is used widely together with other RGD peptides in integrin research. GRGDSP can be used to modify the surface of cardiovascular implants such as vascular grafts to promote endothelialization[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
701.61
Formula
C24H38F3N9O12
Sequence
Gly-Arg-Gly-Asp-Ser-Pro
Sequence Shortening
GRGDSP
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Qian J, et al. Transarterial administration of integrin inhibitor loaded nanoparticles combined with transarterial chemoembolization for treating hepatocellular carcinoma in a rat model. World J Gastroenterol. 2016 Jun 7;22(21):5042-9.
[2]. Patel S, et al. Regulation of endothelial cell function by GRGDSP peptide grafted on interpenetrating polymers. J Biomed Mater Res A. 2007 Nov;83(2):423-33.
PKA Inhibitor Fragment (6-22) amide TFA;(Synonyms: PKI-(6-22)-amide TFA) 纯度: 96.71%
PKA Inhibitor Fragment (6-22) amide TFA 是 cAMP 依赖性蛋白激酶 A (PKA) 的抑制剂，Ki 值为 2.8 nM。PKA Inhibitor Fragment (6-22) amide TFA 可显着逆转小鼠低水平的吗啡缓解疼痛的感受性。
PKA Inhibitor Fragment (6-22) amide TFA Chemical Structure
规格
价格
是否有货
数量
5 mg
￥2100
In-stock
10 mg
￥3500
In-stock
50 mg
;
询价
;
100 mg
;
询价
;
* Please select Quantity before adding items.
PKA Inhibitor Fragment (6-22) amide TFA 相关产品
bull;相关化合物库:
Bioactive Compound Library Plus
Peptide Library
生物活性
PKA Inhibitor Fragment (6-22) amide TFA is an inhibitor of cAMP-dependent protein kinase A (PKA), with a Ki of 2.8 nM. PKA Inhibitor Fragment (6-22) amide TFA can significantly reverse low-level morphine antinociceptive tolerance in mice[1][2].
IC50 Target
PKA
2.8 nM (Ki)
分子量
1982.08
Formula
C82H131F3N28O26
Sequence Shortening
TYADFIASGRTGRRNAI-NH2
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Katz BM, et, al. Synthesis, characterization and inhibitory activities of (4-N3[3,5-3H]Phe10)PKI(6-22)amide and its precursors: photoaffinity labeling peptides for the active site of cyclic AMP-dependent protein kinase. Int J Pept Protein Res. 1989 Jun;33(6):439-45.
[2]. Dalton GD, et, al. Alterations in brain Protein Kinase A activity and reversal of morphine tolerance by two fragments of native Protein Kinase A inhibitor peptide (PKI). Neuropharmacology. 2005 Apr; 48(5): 648-57.
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.
FSL-1 TFA, a bacterial-derived toll-like receptor 2/6 (TLR2/6) agonist, enhances resistance to experimental HSV-2 infection[1]. FSL-1 TFA induces MMP-9 production through TLR2 and NF-κB/AP-1 signaling pathways in monocytic THP-1 cells[2].
IC50 Target[1][2]
TLR2
;
TLR6
;
MMP-9
;
体外研究 (In Vitro)
FSL-1 significantly reduces HSV-2 replication in human vaginal epithelial cells (EC)[1]. FSL-1 induces significant resistance to experimental genital HSV-2 infection through elaboration of a specific cytokine response profile[1]. FSL-1 (50 ng/mL, 24 hours) induces MMP-9 expression at both mRNA and protein levels in human monocytic THP-1 cells[2]. FSL-1 activates the MAP kinase/NF-κB signaling pathway[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[1]
Cell Line:
V11I, V12I or V19I immortalized human vaginal EC
Concentration:
6 μg or 0.1 μg
Incubation Time:
Added at 24, 6 or just prior to HSV-2 inoculation (104pfu/well)
Result:
The 6 μg does produced significant reductions when delivered at 24 or 6 h prior to HSV-2 inoculation. The 0.1 μg dose produced reduced HSV-2 replication at 24 or 6 h prior to viral challenge.
体内研究 (In Vivo)
FSL-1 application significantly protectes against genital HSV-2 challenge in mice[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female Swiss-Webster mice (weighing 20-25 g)[1]
Dosage:
2 or 6 μg
Administration:
Delivered vaginally using a positive displacement pipet, prior to or following viral challenge as specified for each experiment.
Result:
The 2 μg does delivered 6 h prior to HSV-2 challenge increased the ID50 (260 pfu) and LD50 (660 pfu) by 10-fold compared to DPBS vehicle control. The single 6 μg dose produced significantly improved outcomes compared to DPBS vehicle application.
分子量
1780.18
Formula
C82H141F3N14O20S
Sequence Shortening
S-(2, 3-Bispalmitoyloxypropyl)-CGDPKHPKSF
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Sealed storage, away from moisture and light
Powder
-80deg;C
2 years
-20deg;C
1 year
*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (sealed storage, away from moisture and light)
Solvent Solubility
In Vitro:;
H2O
Peptide Solubility and Storage Guidelines:
1.;;Calculate the length of the peptide.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. William A Rose 2nd, et al. FSL-1, a bacterial-derived toll-like receptor 2/6 agonist, enhances resistance to experimental HSV-2 infection. Virol J. 2009 Nov 10;6:195.
ATI-2341 is a potent and functionally selective allosteric agonist of C-X-C chemokine receptor type 4 (CXCR4), which functions as a biased ligand, favoring Gαi activation over Gα13. ATI-2341 activates the inhibitory heterotrimeric G protein (Gi) to promote inhibition of cAMP production and induce calcium mobilization. ATI-2341 is a potent and efficacious mobilizer of bone marrow polymorphonuclear neutrophils (PMNs) and hematopoietic stem and progenitor cells (HSPCs)[1][2].
体外研究 (In Vitro)
CXCR4[1]
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
2370.84
Formula
C106H179F3N26O27S2
Sequence Shortening
1-Oxohexadecyl-MGYQKKLRSMTDKYRL
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Quoyer J, et al. Pepducin targeting the C-X-C chemokine receptor type 4 acts as a biased agonist favoring activation of the inhibitory G protein. Proc Natl Acad Sci U S A. 2013 Dec 24;110(52):E5088-97.
[2]. Tchernychev B, et al. Discovery of a CXCR4 agonist pepducin that mobilizes bone marrow hematopoietic cells. Proc Natl Acad Sci U S A. 2010 Dec 21;107(51):22255-9.
Dynorphin A (1-10) (TFA) 是一种内源性的阿片样神经肽，与 κ 阿片受体 (κ-opioid receptor) 结合。Dynorphin A (1-10) (TFA) 也阻断 NMDA 激活的电流，IC50 为 42.0 μM。
Dynorphin A (1-10) (TFA) Chemical Structure
规格
价格
是否有货
数量
1 mg
￥1100
In-stock
5 mg
￥3600
In-stock
10 mg
￥5600
In-stock
50 mg
;
询价
;
100 mg
;
询价
;
* Please select Quantity before adding items.
Dynorphin A (1-10) (TFA) 相关产品
bull;相关化合物库:
Bioactive Compound Library Plus
Peptide Library
生物活性
Dynorphin A (1-10) (TFA), an endogenous opioid neuropeptide, binds to extracellular loop 2 of the κ-opioid receptor. Dynorphin A (1-10) (TFA) also blocks NMDA-activated current with an IC50 of 42.0 μM.
Dynorphin A (1-10) (TFA), an endogenous opioid neuropeptide, binds in the transmembrane domain of the κ-receptor[1]. The non-opioid actions of various forms of Dynorphin A (DynA) are examined on N-methyl-D-aspartate (NMDA) receptor channels in isolated rat trigeminal neurons using the whole-cell patch recording technique. All the dynorphins tested blocked NMDA-activated currents. The blocking actions are voltage-independent. The IC50 is 42.0 μM for DynA(1-10). To determine if shorter dynorphins have the similar blocking property, we examined the action of DynA(1-10) at different membrane potentials. DynA(1-10) blocks INMDA to a similar extent as the membrane potentials changed from -80 to +60 mV. Thus, despite a 160-fold difference in the apparent affinities, DynA(1-32) and DynA(1-10) both exert voltage-independent actions on NMDA receptors[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
1348.48
Formula
C59H92F3N19O14
Sequence
Tyr-Gly-Gly-Phe-Leu-Arg-Arg-Ile-Arg-Pro
Sequence Shortening
YGGFLRRIRP
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Paterlini G, et al. Molecular simulation of dynorphin A-(1-10) binding to extracellular loop 2 of the kappa-opioidreceptor. A model for receptor activation. J Med Chem. 1997 Sep 26;40(20):3254-62.
[2]. Chen L, et al. Dynorphin block of N-methyl-D-aspartate channels increases with the peptide length. J Pharmacol Exp Ther. 1998 Mar;284(3):826-31.
DTP3 TFA is a potent and selective GADD45β/MKK7 (growth arrest and DNA-damage-inducible β/mitogen-activated protein kinase kinase 7) inhibitor. DTP3 TFA targets an essential, cancer-selective cell-survival module downstream of the NF-κB pathway[1].
IC50 Target
GADD45β/MKK7[1]
体外研究 (In Vitro)
DTP3 (10 μM; 1-21 days) causes the potent and tumor-selective induction of JNK activation and apoptosis, as shown by the appearance of phosphorylated JNK, as early as 24 hours[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[2]
Cell Line:
Multiple myeloma (MM) cell lines
Concentration:
10 μM
Incubation Time:
1, 3, 5, 14, 21 days
Result:
Caused the appearance of phosphorylated JNK, as early as 24 hours.
体内研究 (In Vivo)
DTP3 TFA (s.c.; 14.5 mg/kg/day; 28 days) has shown a dramatic shrinkage of the tumors, and virtually eradicates established subcutaneous myeloma xenografts in mice[2]. DTP3 TFA (intravenous injection; 10 mg/kg/day) has t1/2 of 1.26 hours, CL of 27.13 ML/min/kg, and Vd of 2.80 L/kg[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
6 to 8-week old male NOD/SCID mice (NOD.CB17-Prkdcscid/IcrCrl; Charles River)[2]
Dosage:
14.5 mg/kg
Administration:
S.c.; daily; 28 days
Result:
Had shown a dramatic shrinkage of the tumors.
Animal Model:
CD1 male mice of 25-30 g[2]
Dosage:
10 mg/kg (Pharmacokinetic Study)
Administration:
Intravenous injection
Result:
Had t1/2 of 1.26 hours, CL of 27.13 ML/min/kg, and Vd of 2.80 L/kg.
分子量
639.62
Formula
C28H36F3N7O7
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Sealed storage, away from moisture and light
Powder
-80deg;C
2 years
-20deg;C
1 year
*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (sealed storage, away from moisture and light)
溶解性数据
In Vitro:;
H2O : 100 mg/mL (156.34 mM; Need ultrasonic)
DMSO : 50 mg/mL (78.17 mM; Need ultrasonic)
配制储备液
浓度溶剂体积质量
1 mg
5 mg
10 mg
1 mM
1.5634 mL
7.8171 mL
15.6343 mL
5 mM
0.3127 mL
1.5634 mL
3.1269 mL
10 mM
0.1563 mL
0.7817 mL
1.5634 mL
*
请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
In Vivo:
请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：
[1]. Tornatore L, et al. Preclinical toxicology and safety pharmacology of the first-in-class GADD45β/MKK7inhibitor and clinical candidate, DTP3. Toxicol Rep. 2019 Apr 19;6:369-379.
[2]. Tornatore L, et al. Cancer-selective targeting of the NF-κB survival pathway with GADD45β/MKK7 inhibitors. Cancer Cell. 2014 Oct 13;26(4):495-508.
[1]. FEBS Lett. 1995 Jan 2;357(1):93-7. Onogi T, et al. DAMGO, a mu-opioid receptor selective agonist, distinguishes between mu- and delta-opioid receptors around their first extracellular loops.
Caloxin 2A1 TFA is an extracellular plasma membrane Ca2+-ATPase (PMCA) peptide inhibitor. Caloxin 2A1 TFA does not affect basal Mg2+-ATPase or Na+-K+-ATPase[1].
体外研究 (In Vitro)
Caloxin 2A1 TFA inhibits Ca2+-Mg2+-ATPase in human erythrocyte leaky ghosts, but it does not affect basal Mg2+-ATPase or Na+-K+-ATPase in the ghosts or Ca2+-Mg2+-ATPase in the skeletal muscle sarcoplasmic reticulum. Caloxin 2A1 TFA also inhibits Ca2+-dependent formation of the 140-kDa acid-stable acylphosphate[1]. Caloxin 2A1 TFA increases airway smooth muscle cells (ASMCs) apoptosis[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
1592.54
Formula
C66H92F3N19O24
Sequence Shortening
VSNSNWPSFPSSGGG-NH2
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. J Chaudhary, et al. Caloxin: a novel plasma membrane Ca2+ pump inhibitor. Am J Physiol Cell Physiol. 2001 Apr;280(4):C1027-30.
[2]. Yi-fei Chen, et al. Plasma membrane Ca2+-ATPase regulates Ca2+ signaling and the proliferation of airway smooth muscle cells. Eur J Pharmacol. 2014 Oct 5;740:733-41.
