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| CAS:1234319‑68‑6:TAK‑448 | |
| TAK‑448 is a new‑generation highly active kisspeptin receptor agonist peptide. It binds and activates G protein‑coupled KISS1R receptors with high affinity, initially stimulates gonadotropin‑releasing hormone secretion, while sustained administration induces receptor desensitization, downregulates the hypothalamic‑pituitary‑gonadal axis function, and significantly inhibits the synthesis and secretion of sex hormones such as testosterone and estrogen. With strong anti‑proteolytic ability and long in vivo half‑life after structural modification, it is a novel tool peptide for prostate cancer, sex hormone‑dependent diseases and reproductive endocrine research. | |
| 95%/98%/99% | |
| ~1300 (subject to actual synthetic batch) | |
| Function Tags (comma-separated) | ||||||||
| TAK-448 | TAK-448; Kisspeptin agonist | KISS1R agonism, Sex hormone secretion inhibition, Prostate cancer research, Reproductive endocrinology, Long-acting stable, Modified peptide | Kisspeptin-10 homologous backbone with multi-site modifications for optimized receptor affinity and metabolic stability | - | ~1300 (theoretical) | Unnatural amino acid substitution + terminal modification | 10 |
| Long-term Storage | Short-term Storage | ||||
| PEP-TAK001 | Store at -20℃, sealed, dry & protected from light, aliquoted; avoid repeated freeze-thaw cycles | Stable for 1 month at 2-8℃ sealed & dry; ice pack shipping recommended | Stable for 7 days at 4℃; stable for 1 month at -20℃ in aliquots. **Moderate water solubility, soluble in dilute acetic acid or weakly acidic buffer**. Anti-enzymatic ability significantly better than native kisspeptin after modification | Stable for 3 years at -20℃ under dry & dark conditions |
| Applicable Research Areas (comma-separated) | ||||
| PEP-TAK001 | Long-acting KISS1R agonist peptide that induces receptor desensitization with sustained administration and potently inhibits gonadal axis and sex hormone secretion | TAK-448 activates the Gq/PLC/IP3/Ca²⁺ signaling pathway by highly specifically binding KISS1R receptors on the surface of hypothalamic GnRH neurons. Pulsed initial administration stimulates GnRH and gonadotropin secretion; sustained administration leads to receptor internalization and desensitization, reversibly inhibits hypothalamic-pituitary-gonadal axis function, significantly reduces circulating testosterone and estrogen levels, and exerts a pharmacological castration effect. Compared with native kisspeptin, its ability to resist peptidase degradation is greatly improved after multi-site modification, with significantly prolonged in vivo half-life and more durable effect. It is an efficient tool for sex hormone-dependent diseases and reproductive endocrine research. | Prostate cancer research, Sex hormone-dependent diseases, Reproductive endocrine mechanism, Pubertal development regulation, Pharmacological castration research, Peptide drug development | Kisspeptin Receptor (KISS1R/GPR54); GnRH/gonadotropin secretion pathway; Hypothalamic-pituitary-gonadal axis regulatory pathway |
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