Kisspeptin-10 25 mg


CAS No: 374675-21-5

Purity: 98%

Molar Mass:1302.00

Chemical Formula:C63H83N17O14


Kisspeptin-10 25 mg $295.00

Product Name: Kisspeptin-10

CAS No: 374675-21-5

CAT No: P100119

Molar Mass: 1302.00

Chemical Formula: C63H83N17O14

Synonyms: Metastin (45-54)

Storage:Store at -20°C


Target: GPR54

Purity: 98%


Kisspeptin-10 is a synthetic peptide derived from the kisspeptin protein, which plays a crucial role in regulating reproductive function by stimulating the release of gonadotropin-releasing hormone (GnRH). In pharmaceutical chemistry, Kisspeptin-10 is investigated for its potential therapeutic applications in the management of reproductive disorders, such as infertility and delayed puberty. It acts as a potent stimulator of the reproductive axis, promoting the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland, which are essential for ovulation and spermatogenesis. Additionally, Kisspeptin-10 is studied for its role in modulating the menstrual cycle and enhancing fertility treatments, such as in vitro fertilization (IVF) and assisted reproductive technologies. Its mechanism of action in regulating reproductive function highlights its potential as a novel therapeutic target for addressing various reproductive health concerns in both men and women.

Current Research:

As aging progresses, bone metabolism undergoes changes favoring over-activation of osteoclasts, leading to bone loss, a common feature of diseases like osteoporosis. Osteoclast formation is induced by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL), which promote actin remodeling and bone resorption, primarily mediated by Src kinase activation. Src, activated through auto-phosphorylation at tyrosine 416, plays a crucial role in osteoclast function, as evidenced by severe osteopetrosis in Src gene knockout mice. Thus, targeting Src kinase activity has emerged as a potential therapeutic strategy for osteoclast-related bone loss.

G protein-coupled receptors (GPCRs), major drug targets, regulate Src kinase activity through various mechanisms. GPR54, also known as KiSS1 receptor, is a GPCR activated by its ligands, Kisspeptins, including Kisspeptin-10 (Kp-10). While Kisspeptin/GPR54 signaling regulates puberty via the hypothalamic-pituitary-gonadal axis, its role in bone metabolism has been less explored. Our study reveals that upon activation by Kp-10, GPR54 recruits active Src and the phosphatase Dusp18 via a conserved proline-rich (PR) motif in its C-terminus. This recruitment leads to the dephosphorylation of Src at Y416 by Dusp18, negatively regulating osteoclast activities. In vivo studies using knockout mice confirm the bone protective role of Kp-10/GPR54 signaling, with both whole-body and osteoclast-specific knockout mice exhibiting bone loss and osteoclast hyperactivation. Additionally, a bone-targeting derivative of Kp-10, (DSS)6-Kp-10, demonstrates efficacy in protecting against bone loss in an osteoporosis model induced by ovariectomy.

Evolutionary analysis suggests that the PR motif in the GPR54 C-terminus emerged during the transition from aquatic to terrestrial life, possibly indicating its role in modulating Src activity in osteoclasts. The dosage-dependent effects of Kp-10/GPR54 signaling on Src phosphorylation highlight the complexity of GPCR signaling and its implications for therapeutic interventions. Moreover, the interplay between Kisspeptin/GPR54 signaling and the hypothalamic-pituitary-gonadal axis underscores the multifaceted roles of these molecules in regulating bone metabolism.

In conclusion, our findings shed light on the molecular mechanisms underlying the regulation of osteoclast activities by Kisspeptin/GPR54 signaling. Targeting this pathway, particularly with bone-targeting Kp-10 derivatives, holds promise for the development of novel therapies for osteoclast-associated bone loss disorders like osteoporosis. Further elucidation of the intricate signaling networks involving GPCRs and Src kinase will provide insights into the pathophysiology of bone diseases and facilitate the development of targeted therapeutic interventions.


Li, Z., Yang, X., Fu, R., Wu, Z., Xu, S., Jiao, J., … & Xiao, J. (2024). Kisspeptin-10 binding to Gpr54 in osteoclasts prevents bone loss by activating Dusp18-mediated dephosphorylation of Src. Nature Communications, 15(1), 1-17.

Cao, Y., Hu, G., Zhang, Q., Ma, L., Wang, J., Li, W., … & Liu, J. (2021). Kisspeptin-10 maintains the activation of the mTOR signaling pathway by inhibiting SIRT6 to promote the synthesis of milk in bovine mammary epithelial cells. Journal of Agricultural and Food Chemistry, 69(14), 4093-4100.