Cortistatin 14Endogenous neuropeptide; binds ghrelin receptor and sst1 - sst5 CAS# 193829-96-8 |
- CZC24832
Catalog No.:BCC1507
CAS No.:1159824-67-5
- PI3Kγ inhibitor 1
Catalog No.:BCC4180
CAS No.:1172118-03-4
- CAL-130
Catalog No.:BCC1440
CAS No.:1431697-74-3
- A-443654
Catalog No.:BCC1321
CAS No.:552325-16-3
- CAL-101 (Idelalisib, GS-1101)
Catalog No.:BCC1270
CAS No.:870281-82-6
- BKM120
Catalog No.:BCC1279
CAS No.:944396-07-0
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 193829-96-8 | SDF | Download SDF |
PubChem ID | 16133803 | Appearance | Powder |
Formula | C81H113N19O19S2 | M.Wt | 1721.03 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 0.70 mg/ml in water | ||
Sequence | PCKNFFWKTFSSCK (Modifications: Disulfide bridge between 2 - 13) | ||
SMILES | CC(C1C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(CSSCC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)N1)CCCCN)CC2=CNC3=CC=CC=C32)CC4=CC=CC=C4)CC5=CC=CC=C5)CC(=O)N)CCCCN)NC(=O)C6CCCN6)C(=O)NC(CCCCN)C(=O)O)CO)CO)CC7=CC=CC=C7)O | ||
Standard InChIKey | DDRPLNQJNRBRNY-WYYADCIBSA-N | ||
Standard InChI | InChI=1S/C81H113N19O19S2/c1-46(103)67-80(117)95-59(38-49-24-9-4-10-25-49)73(110)96-62(42-101)76(113)97-63(43-102)77(114)99-65(79(116)90-56(81(118)119)30-15-18-34-84)45-121-120-44-64(98-68(105)53-31-19-35-86-53)78(115)89-54(28-13-16-32-82)69(106)94-61(40-66(85)104)75(112)92-57(36-47-20-5-2-6-21-47)71(108)91-58(37-48-22-7-3-8-23-48)72(109)93-60(39-50-41-87-52-27-12-11-26-51(50)52)74(111)88-55(70(107)100-67)29-14-17-33-83/h2-12,20-27,41,46,53-65,67,86-87,101-103H,13-19,28-40,42-45,82-84H2,1H3,(H2,85,104)(H,88,111)(H,89,115)(H,90,116)(H,91,108)(H,92,112)(H,93,109)(H,94,106)(H,95,117)(H,96,110)(H,97,113)(H,98,105)(H,99,114)(H,100,107)(H,118,119)/t46-,53+,54+,55+,56+,57+,58+,59+,60+,61+,62+,63+,64+,65+,67+/m1/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Endogenous neuropeptide, mainly expressed in the cortex and hippocampus, that has structural and functional similarities to somatostatin-14. Displays potency at all somatostatin receptors (sst1 - sst5) and prevents somatostatin-14 binding (IC50 values are 5, 0.09, 0.3, 0.2 and 0.3 nM at sst1, sst2, sst3, sst4 and sst5 receptors respectively). Also binds to the growth hormone secretagog receptor (GHS-R1a). Exhibits neuronal depressant and sleep-modulating properties in vivo. |
Cortistatin 14 Dilution Calculator
Cortistatin 14 Molarity Calculator
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
- SB 242235
Catalog No.:BCC4171
CAS No.:193746-75-7
- Aminoguanidine hydrochloride
Catalog No.:BCC6795
CAS No.:1937-19-5
- 8beta-Methoxyatractylenolide I
Catalog No.:BCN7594
CAS No.:193694-24-5
- Methyl 4-hydroxycinnamate
Catalog No.:BCN4014
CAS No.:19367-38-5
- TAS 301
Catalog No.:BCC6214
CAS No.:193620-69-8
- BRL-15572
Catalog No.:BCC5065
CAS No.:193611-72-2
- SB 216641 hydrochloride
Catalog No.:BCC6987
CAS No.:193611-67-5
- Terrestrosin K
Catalog No.:BCN2935
CAS No.:193605-07-1
- GB 1b
Catalog No.:BCN7385
CAS No.:19360-72-6
- Calcifediol
Catalog No.:BCC4949
CAS No.:19356-17-3
- SB 239063
Catalog No.:BCC1923
CAS No.:193551-21-2
- IPAG
Catalog No.:BCC5662
CAS No.:193527-91-2
- Tinidazole
Catalog No.:BCC4866
CAS No.:19387-91-8
- Fmoc-β-Homo-Leu-OH
Catalog No.:BCC2631
CAS No.:193887-44-4
- 3-Phenyl-1,2-dihydroacenaphthylene-1,2-diol
Catalog No.:BCN7178
CAS No.:193892-33-0
- SC 19220
Catalog No.:BCC6968
CAS No.:19395-87-0
- Fmoc-ß-HoAla-OH
Catalog No.:BCC3225
CAS No.:193954-26-6
- Fmoc- ß-HoIle-OH
Catalog No.:BCC3237
CAS No.:193954-27-7
- Fmoc-β-HoPhe-OH
Catalog No.:BCC3241
CAS No.:193954-28-8
- 10-O-Vanilloylaucubin
Catalog No.:BCN1185
CAS No.:193969-08-3
- Cedrelopsin
Catalog No.:BCN7687
CAS No.:19397-28-5
- 6,19-Dihydroxyurs-12-en-3-oxo-28-oic acid
Catalog No.:BCN1513
CAS No.:194027-11-7
- 3-Amino-4-methylbenzamide
Catalog No.:BCC8614
CAS No.:19406-86-1
- Dihydrocapsaicin
Catalog No.:BCN1017
CAS No.:19408-84-5
The activation of somatostatinergic receptors by either somatostatin-14 or cortistatin-17 often inhibits ACTH hypersecretion in patients with Cushing's disease.[Pubmed:17893252]
Eur J Endocrinol. 2007 Oct;157(4):393-8.
OBJECT: Somatostatin (SS) is known to inhibit GH and insulin, while its effect on corticotrope secretion is controversial: inhibition of ACTH secretion by agonists activating somatostatinergic receptors (sst)-2 and sst-5 was reported in vitro. Cortistatin (CST) not only binds all sst receptor subtypes but also possesses central actions that are not shared by SS. DESIGN: In nine patients with Cushing's disease (CD), ACTH, cortisol, GH, insulin, and glucose levels were studied during 120-min i.v. infusion of SS-14 (2.0 microg/kg per h), CST-17 (2.0 microg/kg per h) or saline. RESULTS: Both SS or CST significantly affected the hypothalamic-pituitary-adrenal axis. Cortisol was decreased to the same extent by either SS or CST (P < 0.05). Both SS and CST decreased ACTH, although statistical difference was reached only during CST (P < 0.05). Analyzing the individual responses as areas under curve (AUCs), a clear and consensual inhibition of ACTH and cortisol under either SS or CST was recorded in five out of nine patients. Both SS or CST inhibited (P < 0.05) insulin, that even showed a rebound (P < 0.01) at the end of infusion. GH was not modified by either peptide. CONCLUSION: SS and CST often display similar inhibitory effects on the HPA axis in CD. The activation of sst receptors by both peptides is followed in almost 50% of patients by a remarkable inhibition of ACTH and cortisol hypersecretion. These findings reinforce the view that sst receptors are involved in the control of the secretory activity of tumoral corticotropic cells.
Comparison of the anti-inflammatory and anti-nociceptive effects of cortistatin-14 and somatostatin-14 in distinct in vitro and in vivo model systems.[Pubmed:21695504]
J Mol Neurosci. 2012 Jan;46(1):40-50.
We showed that somatostatin (SST) exerts anti-inflammatory and anti-nociceptive effects through somatostatin receptor subtypes 4 and 1 (sst(4)/sst(1)). Since cortistatin (CST) is a structurally similar peptide, we aimed at comparing the sst(1)- and sst(4)-binding and activating abilities, as well as the effects of SST-14 and CST-14 on inflammatory and nociceptive processes. CST-14 concentration-dependently displaced radiolabeled SST-14 binding, induced similar sst(1) and sst(4)-activation with a less potency, and exerted significantly greater inhibitory effect on endotoxin-stimulated interleukin (IL)-1beta production of murine peritoneal macrophages. Capsaicin-induced calcitonin gene-related peptide release from peripheral sensory nerve terminals of isolated rat tracheae was significantly decreased by 2 muM CST and 100 nM SST, but concentration-response correlation was not found. Mustard oil-evoked acute neurogenic plasma protein extravasation in the rat hindpaw skin, carrageenan-induced mouse paw edema, mechanical hyperalgesia, and IL-1beta, tumor necrosis factor-alpha production, as well as mild heat injury-evoked thermal hyperalgesia were similarly attenuated by both peptides. In the latter case, i.pl. and i.p. injections exerted equal inhibitory actions. CST-14 and SST-14 similarly diminish both acute neurogenic and cellular inflammatory processes, as well as mechanical and heat hyperalgesia, in which their inhibitory effect on sensory nerve endings is likely to be involved. However, CST-14 exerts remarkably greater inhibition on cytokine production.
Cortistatin-17 and somatostatin-14 display the same effects on growth hormone, prolactin, and insulin secretion in patients with acromegaly or prolactinoma.[Pubmed:16449338]
J Clin Endocrinol Metab. 2006 Apr;91(4):1595-9.
CONTEXT: Cortistatin binds all somatostatin receptor subtypes but also has particular central actions; moreover, a specific cortistatin receptor has also been discovered. OBJECTIVE: We compared the endocrine effects of cortistatin-17 with those of somatostatin-14 in patients with acromegaly (ACRO) or prolactinoma (PRLOMA). Normal subjects (NS) were studied as control group. DESIGN: All subjects underwent the following tests: 1) saline, 2) somatostatin-14 (2.0 microg/kg.h iv, 0-120 min) and 3) cortistatin-17 (2.0 microg/kg.h iv, 0-120 min) infusion. RESULTS: Cortistatin-17 and somatostatin-14 inhibited GH secretion to the same extent in ACRO (P < 0.05) and NS (P < 0.01). Cortistatin-17 and somatostatin-14 inhibited PRL secretion in PRLOMA (P < 0.05), to some extent in ACRO (P value not significant), but not in NS. Insulin secretion was inhibited by both cortistatin-17 and somatostatin-14 to the same extent in all groups (P < 0.05). CONCLUSIONS: Cortistatin-17 and somatostatin-14 display the same effects on GH, PRL, and insulin secretion in patients with ACRO or PRLOMA.
Cortistatin-14 mediates its anticonvulsant effects via sst2 and sst3 but not ghrelin receptors.[Pubmed:24685142]
CNS Neurosci Ther. 2014 Jul;20(7):662-70.
Cortistatin (CST)-14, a neuropeptide that is structurally and functionally related to somatostatin-14 (SRIF) binds all five somatostatin receptor subtypes (sst1-sst5). Using in vivo microdialysis and telemetry-based electroencephalographic recordings, we provide the first experimental evidence for anticonvulsive effects of CST-14 in a pilocarpine-induced seizure model in rats and mice and for the involvement of sst2 and sst3 receptors in these anticonvulsant actions of CST-14. Both receptor subtypes are required for the anticonvulsant effects of CST-14 given that co-perfusion of a selective sst2 antagonist (cyanamid15486) or a selective sst3 antagonist (SST3-ODN-8) reversed anticonvulsant effect of CST-14, and this, independently of each other. Next, as the ghrelin receptor has been proposed as a target for the biological effects of CST-14, we used ghrelin receptor knockout mice and their wild type littermates to study the involvement of this receptor in the anticonvulsive actions of CST-14. Our results show a significant decrease in seizure duration in both genotypes when CST-14 treated mice were compared with corresponding control animals receiving only pilocarpine. In addition, this CST-14-induced decrease was comparable in both genotypes. We here thus provide the first evidence that ghrelin receptors are not involved in mediating anticonvulsant actions of CST-14 in vivo.
Cortistatin, but not somatostatin, binds to growth hormone secretagogue (GHS) receptors of human pituitary gland.[Pubmed:11227737]
J Endocrinol Invest. 2001 Jan;24(1):RC1-3.
Antagonism between GH secretagogues (GHS) and somatostatin (SRIH) has been postulated and demonstrated, but SRIH does not bind to GHS receptors (GHS-R) and potent synthetic peptidyl GHS (GHRP6, hexarelin) do not displace radiolabeled SRIH from its receptors. However, non-natural SRIH octapeptide agonists (mainly lanreotide and vapreotide) displace 125I-Tyr-Ala-hexarelin from pituitary binding sites suggesting that an endogenous factor related to SRIH might exist and interact with GHS-R. Our aims were to investigate the ability of different SRIH-like peptides such as various SRIH fragments (SRIH 3-14, SRIH 7-14, SRIH 3-10, SRIH 7-10, SRIH 2-9) and a natural neuropeptide that shows a high structural homology with SRIH such as cortistatin-14 (CST) to compete with 125I-Tyr-Ala-hexarelin for human pituitary binding sites and to compare their binding affinity with that of hexarelin and ghrelin, a gastric-derived peptidyl GHS that has been proposed as a natural ligand of GHS-R. While the binding of 125I-Tyr-Ala-hexarelin to pituitary membranes was completely displaced by unlabelled hexarelin, ghrelin and CST, none of the SRIH fragments tested inhibited this binding. Ghrelin and CST exhibited a similar affinity (4.6-5.4 x 10(-7) mol/l) for the binding while hexarelin was more effective by about four orders of magnitude in displacing 125I-Tyr-Ala-hexarelin. Our data demonstrate for the first time that cortistatin, a natural peptide related to SRIH, binds to GHS-R and suggest that this factor may play a role in modulating the activity of these receptors.