Comparison
Kisspeptin-10 vs. Teriparatid
Two peptides side-by-side — identity, evidence base, legal status and known adverse events.
Identity
Category
Research other
Research other
CAS no.
374675-21-5
52232-67-4
Molecular weight
1302.44 g/mol
4117.8 g/mol
Half-life
0.07 h
1 h
Sequence
H-Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2Ser-Val-Ser-Glu-Ile-Gln-Leu-Met-His-Asn-Leu-Gly-Lys-His-Leu-Asn-Ser-Met-Glu-Arg-Val-Glu-Trp-Leu-Arg-Lys-Lys-Leu-Gln-Asp-Val-His-Asn-PheMechanism of action
Kisspeptin-10
Kisspeptin-10 comprises the ten C-terminal amino acids sufficient for binding to the KISS1R receptor (also GPR54). KISS1R is a G-protein-coupled receptor expressed predominantly on GnRH neurons in the hypothalamus. Activation signals through the Gq/11-phospholipase C pathway to release gonadotropin-releasing hormone (GnRH), which in turn drives the pituitary to secrete luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Kisspeptin signaling is regarded as an indispensable trigger of puberty; inactivating mutations in KISS1R are associated with absent puberty (idiopathic hypogonadotropic hypogonadism). Beyond the reproductive axis, KISS1R expression is described in limbic brain regions, discussed as a possible mechanism for the effects on sexual and emotional processing observed in imaging studies.
Teriparatid
Teriparatide corresponds to the biologically active first 34 amino acids of human parathyroid hormone and binds the PTH-1 receptor on bone and kidney cells. The literature describes that intermittent receptor activation preferentially stimulates the activity of bone-forming osteoblasts, whereas continuously elevated PTH exposure (as in hyperparathyroidism) tends to favor bone resorption. This time-dependent difference is regarded as the mechanistic basis for the bone-anabolic effect observed in studies.
Evidence base
Highest evidence
Human RCT
Human RCT
Studies
4
4
of which in humans
4
4
Effects recorded
4
3
Open conflicts
1
1
Documented adverse events
1
2
Legal status
Full entries
Frequently asked questions
- What is the difference between Kisspeptin-10 and Teriparatid?
- Kisspeptin-10 is classified as "Research other", while Teriparatid is classified as "Research other". Kisspeptin-10: Kisspeptin-10 is the shortest bioactive fragment (10 amino acids) of the endogenous neuropeptide kisspeptin, encoded by the KISS1 gene. It acts as an agonist at the KISS1R (GPR54) receptor and stimulates hypothalamic GnRH neurons, driving release of LH and FSH. Kisspeptin is a master switch of puberty and reproduction and is studied in humans, notably by the group of Waljit Dhillo (Imperial College London), in reproductive disorders and in sexual and emotional brain processing. It is not an approved drug. Teriparatid: Teriparatide is the recombinant N-terminal fragment 1-34 of human parathyroid hormone (PTH). It is regulatory-approved and studied in the scientific literature as a bone-anabolic agent for the treatment of osteoporosis. Unlike antiresorptive agents, studies attribute to it an effect that stimulates new bone formation. This page contrasts both neutrally and source-based — with no usage or dosing recommendation.
- Which peptide is better supported by science, Kisspeptin-10 or Teriparatid?
- The highest available evidence level is "Human RCT" for Kisspeptin-10 and "Human RCT" for Teriparatid. A higher evidence level means more robust data, but says nothing about suitability for an individual. The full body of evidence is on each peptide's own page.
- What is the legal status of Kisspeptin-10 and Teriparatid in Germany and the United States?
- Germany: Kisspeptin-10 — Unapproved, Teriparatid — Prescription. United States: Kisspeptin-10 — Research only, Teriparatid — Prescription. These are factual summaries with source and review date on the individual pages.