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Kisspeptin 10 (human)

Endogenous ligand for kisspeptin receptor CAS# 374675-21-5

Kisspeptin 10 (human)

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Chemical structure

Kisspeptin 10 (human)

3D structure

Chemical Properties of Kisspeptin 10 (human)

Cas No. 374675-21-5 SDF Download SDF
PubChem ID 25240297 Appearance Powder
Formula C63H83N17O14 M.Wt 1302.45
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Metastin (45-54), Kp-10
Solubility 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:
3.  Recommended solution:
Sequence YNWNSFGLRF

(Modifications: Phe-10 = C-terminal amide)

Chemical Name (2S)-N-[(2S)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-amino-1-oxo-3-phenylpropan-2-yl]amino]-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]-2-[[(2S)-2-amino-3-(4-hydroxyphenyl)propanoyl]amino]butanediamide
SMILES CC(C)CC(C(=O)NC(CCCN=C(N)N)C(=O)NC(CC1=CC=CC=C1)C(=O)N)NC(=O)CNC(=O)C(CC2=CC=CC=C2)NC(=O)C(CO)NC(=O)C(CC(=O)N)NC(=O)C(CC3=CNC4=CC=CC=C43)NC(=O)C(CC(=O)N)NC(=O)C(CC5=CC=C(C=C5)O)N
Standard InChIKey RITKWYDZSSQNJI-INXYWQKQSA-N
Standard InChI InChI=1S/C63H83N17O14/c1-34(2)24-45(58(90)74-43(18-11-23-70-63(68)69)57(89)75-44(54(67)86)26-35-12-5-3-6-13-35)73-53(85)32-72-56(88)46(27-36-14-7-4-8-15-36)77-62(94)50(33-81)80-61(93)49(30-52(66)84)79-59(91)47(28-38-31-71-42-17-10-9-16-40(38)42)78-60(92)48(29-51(65)83)76-55(87)41(64)25-37-19-21-39(82)22-20-37/h3-10,12-17,19-22,31,34,41,43-50,71,81-82H,11,18,23-30,32-33,64H2,1-2H3,(H2,65,83)(H2,66,84)(H2,67,86)(H,72,88)(H,73,85)(H,74,90)(H,75,89)(H,76,87)(H,77,94)(H,78,92)(H,79,91)(H,80,93)(H4,68,69,70)/t41-,43-,44-,45-,46-,47-,48-,49-,50-/m0/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.

Biological Activity of Kisspeptin 10 (human)

DescriptionPotent endogenous ligand for the Kisspeptin receptor (KISS1, GPR54). Binds with high affinity to rat and human KISS1 receptors with Ki values of 1.59 and 2.33 nM respectively. Inhibits metastasis and invasion in mouse melanomas and stimulates gonadotropin secretion following i.c.v. administration.

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Background on Kisspeptin 10 (human)

Kisspeptin-10 is a potent endogenous agonist for GPR54, used as a vasoconstrictor and an angiogenesis inhibitor. Sequence: Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2.

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].

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.

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References on Kisspeptin 10 (human)

Kisspeptin-10 inhibits stromal-derived factor 1-induced invasion of human endometrial cancer cells.[Pubmed:24407584]

Int J Gynecol Cancer. 2014 Feb;24(2):210-7.

OBJECTIVES: The cross talk between metastatic cancer cells and target sites is critical for the development and progression of metastases. Disruption of this interaction will allow to design mechanism-based effective and specific therapeutic interventions for metastases. We have established a coculture system of cells derived from different tumor entities and MG63 human osteoblastlike cells to analyze tumor cell invasion. Recently, we have shown that breast cancer cell invasion was dramatically increased when cocultured with MG63 cells.Using this model, we have now analyzed whether stromal-derived factor 1 (SDF-1) is responsible for human endometrial cancer cell invasion and whether kisspeptin-10 (KP-10) treatment affects SDF-1-induced invasion of endometrial cancer cells in vitro. METHODS: Invasion was quantified by assessment of endometrial cancer cell migration rate through an artificial basement membrane in a modified Boyden chamber during coculture with MG63 cells or after treatment with SDF-1alpha, SDF-1beta, or the combination of both SDF-1 isoforms. In addition, the role of SDF-1 in invasion of endometrial cancer cells was analyzed by blocking SDF-1 secretion during coculture with MG64 cells. Furthermore, the effects of KP-10 treatment on MG63 coculture-driven and SDF-1-induced invasion were analyzed. RESULTS: Endometrial cancer cell invasion was significantly increased when cocultured with MG63 cells. Treatment with KP-10 reduced the ability to invade a reconstituted basement membrane and to migrate in response to the cellular stimulus. This effect was significant in a dose window of 10(-13) to 10(-11) mol/L. During coculture, SDF-1 protein expression of MG63 cells was significantly increased. The MG63 coculture-induced increase of endometrial cancer cell invasion could be blocked by anti-SDF-1 antibodies. Treatment of endometrial cancer cells in monoculture (without MG63) with SDF-1alpha, SDF-1beta, or the combination of both isoforms resulted in a significant increase of endometrial cancer cell invasion. The SDF-1-induced increase of endometrial cancer cell invasion was significantly reduced after treatment with KP-10. CONCLUSIONS: Our findings suggest that SDF-1 plays a major role in endometrial cancer invasion. Stromal-derived factor 1-induced invasion can be inhibited by KP-10 treatment.

Kisspeptin-10 inhibits angiogenesis in human placental vessels ex vivo and endothelial cells in vitro.[Pubmed:20926586]

Endocrinology. 2010 Dec;151(12):5927-34.

Recent studies suggest that kisspeptin (a neuropeptide central to the regulation of gonadotrophin secretion) has diverse roles in human physiology, including a putative role in implantation and placental function. Kisspeptin and its receptor are present in human blood vessels, where they mediate vasoconstriction, and kisspeptin is known to inhibit tumor metastasis and trophoblast invasion, both processes involving angiogenesis. We hypothesized that kisspeptin contributes to the regulation of angiogenesis in the reproductive system. The presence of the kisspeptin receptor was confirmed in human placental blood vessels and human umbilical vein endothelial cells (HUVEC) using immunochemistry. The ability of kisspeptin-10 (KP-10) (a shorter biologically active processed peptide) to inhibit angiogenesis was tested in explanted human placental arteries and HUVEC using complementary ex vivo and in vitro assays. KP-10 inhibited new vessel sprouting from placental arteries embedded in Matrigel and tube-like structure formation by HUVEC, in a concentration-dependent manner. KP-10 had no effect on HUVEC viability or apoptosis but induced concentration-dependent inhibition of proliferation and migration. In conclusion, KP-10 has antiangiogenic effects and, given its high expression in the placenta, may contribute to the regulation of angiogenesis in this tissue.

Kisspeptin-10, a KiSS-1/metastin-derived decapeptide, is a physiological invasion inhibitor of primary human trophoblasts.[Pubmed:15020672]

J Cell Sci. 2004 Mar 15;117(Pt 8):1319-28.

Trophoblast invasion of the uterine extracellular matrix, a critical process of human implantation and essential for fetal development, is a striking example of controlled invasiveness. To identify molecules that regulate trophoblast invasion, mRNA signatures of trophoblast cells isolated from first trimester (high invasiveness) and term placentae (no/low invasiveness) were compared using U95A GeneChip microarrays yielding 220 invasion/migration-related genes. In this 'invasion cluster', KiSS-1 and its G-protein-coupled receptor KiSS-1R were expressed at higher levels in first trimester trophoblasts than at term of gestation. Receptor and ligand mRNA and protein were localized to the trophoblast compartment. In contrast to KiSS-1, which is only expressed in the villous trophoblast, KiSS-1R was also found in the extravillous trophoblast, suggesting endocrine/paracrine activation mechanisms. The primary translation product of KiSS-1 is a 145 amino acid polypeptide (Kp-145), but shorter kisspeptins (Kp) with 10, 13, 14 or 54 amino acid residues may be produced. We identified Kp-10, a dekapeptide derived from the primary translation product, in conditioned medium of first trimester human trophoblast. Kp-10, but not other kisspeptins, increased intracellular Ca(2+) levels in isolated first trimester trophoblasts. Kp-10 inhibited trophoblast migration in an explant as well as transwell assay without affecting proliferation. Suppressed motility was paralleled with suppressed gelatinolytic activity of isolated trophoblasts. These results identified Kp-10 as a novel paracrine/endocrine regulator in fine-tuning trophoblast invasion generated by the trophoblast itself.

Expression of functional KISS1 and KISS1R system is altered in human pituitary adenomas: evidence for apoptotic action of kisspeptin-10.[Pubmed:21169415]

Eur J Endocrinol. 2011 Mar;164(3):355-62.

CONTEXT: KISS1 was originally identified as a metastasis-suppressor gene able to inhibit tumor progression. KISS1 gene products, the kisspeptins, bind to a G-protein-coupled receptor (KISS1R, formerly GPR54), which is highly expressed in placenta, pituitary, and pancreas, whereas KISS1 mRNA is mainly expressed in placenta, hypothalamus, striatum, and pituitary. OBJECTIVE AND DESIGN: KISS1/KISS1R pituitary expression profile, coupled to their anti-tumoral capacities, led us to hypothesize that this system may be involved in the biology of pituitary tumors. To explore this notion, expression levels of KISS1R and KISS1 were evaluated in normal and adenomatous pituitaries. Additionally, functionality of this system was assessed by treating dispersed pituitary adenoma cells in primary culture with kisspeptin-10 and evaluating intracellular calcium kinetics and apoptotic rate. RESULTS: Both KISS1 and KISS1R were expressed in normal pituitary, whereas this simultaneous expression was frequently lost in pituitary tumors, where diverse patterns of KISS1/KISS1R expression were observed that differed among distinct types of pituitary adenomas. Measurement of calcium kinetics revealed that kisspeptin-10 elicits a remarkable increase in [Ca(2+)](i) in individual cells from four out of the five GH-producing adenomas studied, whereas cells derived from non-functioning pituitary adenomas (NFPA, n=45) did not respond. In contrast, kisspeptin-10 treatment increased the apoptotic rate in cells derived from both GH-producing and NFPA. CONCLUSIONS: These results provide primary evidence that KISS1 and KISS1R expression can be differentially lost in pituitary tumor subtypes, where this system can exert functional, proapoptotic actions, and thereby offer novel insights to investigate the biology and therapeutic options to treat these tumors.

Kisspeptin acts directly and indirectly to increase gonadotropin-releasing hormone neuron activity and its effects are modulated by estradiol.[Pubmed:18162521]

Endocrinology. 2008 Apr;149(4):1979-86.

GnRH neurons play a pivotal role in the central regulation of fertility. Kisspeptin greatly increases GnRH/LH release and GnRH neuron firing activity and may be involved in estradiol feedback, but the neurobiological mechanisms for these actions are unknown. G protein-coupled receptor 54, the receptor for kisspeptin, is expressed by GnRH neurons as well as other hypothalamic neurons, suggesting both direct and indirect effects are possible. To investigate this and determine whether kisspeptin activation of GnRH neurons is estradiol sensitive, we recorded the firing rate of GnRH neurons in brain slices from adult female mice that were ovariectomized (OVX) and either treated with estradiol (E) capsules (OVX+E) or left without further treatment. Kisspeptin increased GnRH neuronal activity in a dose-dependent manner in cells from both OVX and OVX+E mice, and estradiol significantly potentiated the response. To begin to distinguish direct from indirect actions of kisspeptin, fast synaptic transmission mediated by ionotropic gamma-aminobutyric acid and glutamate receptors was pharmacologically blocked (blockade). Blockade reduced GnRH response to kisspeptin in OVX+E but not in OVX mice. Actions of kisspeptin were also assessed using whole-cell voltage- and current-clamp recording in slices from OVX animals. Kisspeptin application depolarized GnRH neurons in current-clamp and generated inward current in voltage-clamp recordings, even after blocking action potential-dependent neural communication, consistent with a direct effect. Blockers of potassium channels abolished the inward current. Together our data indicate that kisspeptin activates GnRH neurons via both direct and transsynaptic mechanisms and that transsynaptic mechanisms are either enabled and/or potentiated by estradiol.

The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54.[Pubmed:11457843]

J Biol Chem. 2001 Sep 14;276(37):34631-6.

Natural peptides displaying agonist activity on the orphan G protein-coupled receptor GPR54 were isolated from human placenta. These 54-, 14,- and 13-amino acid peptides, with a common RF-amide C terminus, derive from the product of KiSS-1, a metastasis suppressor gene for melanoma cells, and were therefore designated kisspeptins. They bound with low nanomolar affinities to rat and human GPR54 expressed in Chinese hamster ovary K1 cells and stimulated PIP(2) hydrolysis, Ca(2+) mobilization, arachidonic acid release, ERK1/2 and p38 MAP kinase phosphorylation, and stress fiber formation but inhibited cell proliferation. Human GPR54 was highly expressed in placenta, pituitary, pancreas, and spinal cord, suggesting a role in the regulation of endocrine function. Stimulation of oxytocin secretion after kisspeptin administration to rats confirmed this hypothesis.

Description

Kisspeptin-10, human is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, human acts as a tumor metastasis suppressor via its receptor GPR54. Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation via NFATc4-mediated BMP2 expression.

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