374675-21-5

374675-21-5 structure

Name: Kisspeptin-13 (4-13) (human) trifluoroacetate salt
Chemical Name: (2S)-N-[(2S)-1-[[(2S)-1-amino-1-oxo-3-phenylpropan-2-yl]amino]-5-(diaminomethylideneamino)-1-oxopentan-2-yl]-4-methyl-2-(methylamino)pentanamide
CAS Number: 374675-21-5
Molecular Formula: C₆₃H₈₃N₁₇O₁₄
Molecular Weight: 1302.44000
Catalog: Peptides
Create Date: 2018-12-30 18:46:00
Modify Date: 2024-01-06 18:17:59
Kisspeptin-10 is a potent endogenous agonist for GPR54, used as a vasoconstrictor and an angiogenesis inhibitor.

Name	(2S)-N-[(2S)-1-[[(2S)-1-amino-1-oxo-3-phenylpropan-2-yl]amino]-5-(diaminomethylideneamino)-1-oxopentan-2-yl]-4-methyl-2-(methylamino)pentanamide
Synonyms	S-Sulfo-L-cysteine sodium salt Kisspeptin-13 (4-13) (human) Kisspeptin-10

Description	Kisspeptin-10 is a potent endogenous agonist for GPR54, used as a vasoconstrictor and an angiogenesis inhibitor.
Related Catalog	Signaling Pathways >> Others >> Others Peptides Research Areas >> Cardiovascular Disease
Target	GPR54[1] Angiogenesis[1]
In Vitro	Kisspeptin-10 (KP-10) significantly increases adhesion of THP-1 cells to HUVECs by 10-fold at 10 μM. Pretreatment with the GPR54 antagonist, P234 (20 μM), significantly inhibits Kisspeptin-10 (10 μM)-induced adhesion of THP-1 cells to HUVECs. These results indicate that Kisspeptin-10 increases the adhesion of THP-1 cells to HUVECs by GPR54. Kisspeptin-10 markedly enhances mRNA expression for TNF-α, IL-6, MCP-1, ICAM-1, VCAM-1, and E-selectin in HUVECs. Kisspeptin-10 significantly increases the protein expression of ICAM-1 and VCAM-1 in HUVECs in parallel with the increases in mRNA levels[1].
In Vivo	The effects of Kisspeptin-10 (KP-10) and the GPR54 antagonist P234 are evaluated on the development of atherosclerotic lesions in 2 different strains of ApoE-/- mice (C57/B6 and BALB/c). In ApoE-/- mice (C57/B6), the (entire) surface and cross-sectional area of the root (plaque size) of aortic atherosclerotic lesions with pentraxin-3-positive area, monocyte/macrophage infiltration, and VSMC content as well as plasma total cholesterol concentration are significantly increased at 17 weeks of age compared with 13 weeks of age. By 17 weeks of age, plasma Kisspeptin-10 concentration is significantly elevated in mice infused with a high dose of Kisspeptin-10 (12.5 μg/kg per hour) compared with the vehicle control. A high dose of Kisspeptin-10 (12.5 μg/kg per hour) significantly enhances the aortic atherosclerotic lesion area and atheromatous plaque size, with significant increases in pentraxin-3-positive area and monocyte/macrophage infiltration and a significant decrease in VSMC content. There are no significant differences in body weight, food intake, systolic and diastolic BP, and plasma concentrations of either total cholesterol or glucose among the 3 groups of ApoE-/- mice at 17 weeks of age[1]. The injection of Kisspeptin-10 can slow down microvascular cutaneous blood flow in mice. The changes in cardiac metabolites in rats treated with Kisspeptin-10 is investigated using a metabonomics approarch based on GC/TOF-MS to the rats. The identification of metabolic pathways and biomarkers may contribute to understanding the mechanism by which Kisspeptin-10 treatment alters cardiac functions. Mitochondria in which energy metabolism occurs is observed through transmission electron microscope (TEM), and the perturbations in energy metabolism can be inferred from changes in mitochondrial structure. There is a clear separation between the control (N) and Kisspeptin-10 (K) groups in the plot regarding serum samples[2].
Cell Assay	HUVECs, HUVEC-derived EA.hy926 cells, or HASMCs at passage 2 to 8 are seeded into 96-well plates (1×104 cells/100 μL/well) and incubated for 24 hours in DMEM or SmGM-2 containing 10% or 5% FBS, respectively. Cells are then incubated for a further 48 hours with the indicated concentrations of Kisspeptin-10 in fresh media. Ten microliters of WST-8 solution are then added to each well. After 1 hour of incubation, the quantity of formazan product is determined by reading absorbance at 450 nm using a Sunrise Remote R-micro plate reader[1].
Animal Admin	Mice[1] A total of 66 of male spontaneously hyperlipidemic ApoE-/- mice in 2 strains, C57/B6 (KOR/StmSlc-Apoeshl mice) and BALB/c (KOR/StmSlc-Apoeshl mice), are used. Mice are fed a high-cholesterol diet containing 16.5% fat, 1.25% cholesterol, and 0.5% sodium cholate, starting at 13 weeks of age. Mice at 13 weeks of age are infused for 4 weeks with Kisspeptin-10 and/or P234, a GPR54 antagonist, using osmotic minipumps. The time course and dose of Kisspeptin-10 and P234 infusion are decided. Experiment 1 is performed to evaluate the dose-dependent effects of Kisspeptin-10 on atherogenesis in 17 ApoE-/- mice (C57BL/6). At 13 weeks of age, 3 mice are euthanized as preinfusion controls. The remaining 14 are divided into 3 groups of 5, 4, and 5 and then infused with saline (vehicle) or Kisspeptin-10 at doses of 5 and 12.5 μg/kg per hour, respectively. Experiment 2 is performed to evaluate the suppressive effects of P234 on Kisspeptin-10-induced atherogenesis in 38 ApoE-/- mice (BALB/c). At 13 weeks of age, 7 mice are euthanized as a control before infusion. The remaining 31 are divided into 3 groups of 10, 10, and 11 and are then infused with saline, Kisspeptin-10 (12.5 μg/kg per hour) or Kisspeptin-10 (12.5 μg/kg per hour)+P234 (50 μg/kg per hour), respectively. Experiment 3 is performed to evaluate the preventive effects of P234 on endogenous Kisspeptin-10-induced atherogenesis (the natural course of atherogenesis) in 10 ApoE-/- mice (BALB/c). From 13 to 17 weeks of age, 5 and 5 mice are infused with saline and P234 (50 μg/kg per hour), respectively[1]. Rats[2] Twenty eight-week-old male Sprague-Dawley rats weighing 200±20 g are used. They are maintained at constant temperature (23±2°C) and humidity (45±15%), with controlled lighting (light 12 h-dark 12 h), and are fed at a standard diet, with free access to tap water. They are adapted to the environment for two weeks to overcome the stress of transportation before the animal experiments began. Then, all of the rats are divided into two groups randomly. Each rat in Kisspeptin-10 group receives subcutaneous injection with 200 μL Kisspeptin-10 (40 nmol/200μL) every day, each rat of the control group receives subcutaneous injection with 200 μL saline every day, both of the two groups are treated for 7 days continuously. Rats are anesthetized with urethane (1.5 g/kg, i.p.). Under general anesthesia, blood samples are collected and rats are euthanized. All efforts are made to minimize the discomfort and stress of animals. Then all the samples are analyzed. Seven days later, the 20 rats are decapitated after exposure to anesthesia. Cardiac tissue and serum samples are collected and stored at -80°C until being used for total RNA and protein extraction as well as metabonomics analysis. The rest of the heart tissue is fixed with 4% paraformaldehyde and 2.5% glutaraldehyde for 24 h at 4°C for further morphological research[2].
References	[1]. Sato K, et al. Potent Vasoconstrictor Kisspeptin-10 Induces Atherosclerotic Plaque Progression and Instability: Reversal by its Receptor GPR54 Antagonist. J Am Heart Assoc. 2017 Apr 14;6(4). pii: e005790. [2]. Zhang Y, et al. The effects of kisspeptin-10 on serum metabolism and myocardium in rats. PLoS One. 2017 Jul 10;12(7):e0179164.

Molecular Formula	C₆₃H₈₃N₁₇O₁₄
Molecular Weight	1302.44000
Exact Mass	1301.63000
PSA	535.34000
LogP	3.51400
Storage condition	2-8℃

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