Hormonal & Reproductive Research

A chemically modified analogue of GHRH(1-29) — the biologically active fragment of endogenous growth hormone-releasing hormone — engineered with four amino acid substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) that resist enzymatic degradation without extending the half-life through albumin binding. Produces a short, sharp physiologic GH pulse. Research-only; no FDA or EMA approval. Distinct from CJC-1295 DAC, which adds an albumin-binding linker and has an ~8-day half-life.

The gold-standard GH secretagogue stack in a single vial: CJC-1295 No DAC 5 mg + Ipamorelin 5 mg = 10 mg total. The two peptides drive growth-hormone release through two distinct receptor systems that are synergistic when combined. CJC-1295 No DAC activates GHRH receptors on pituitary somatotrophs, producing a short, sharp GH pulse. Ipamorelin simultaneously activates ghrelin (GHSR) receptors, amplifying the same GH pulse through a separate pathway. The two signals are synergistic — the combined GH release is significantly greater than the additive sum, because pulsatile activation of both receptor systems produces a physiologic GH pulse larger than either component alone can generate. Ipamorelin does not elevate cortisol, prolactin or ACTH — an important selectivity property that makes this blend cleaner than older ghrelin-mimetic combinations. Both components are optimally dosed at 0.1–0.15 mL per injection, both are well-characterised individually, and both are within their individually-established therapeutic ranges in the blend format.

The identical GHRH(1-29) backbone as CJC-1295 No DAC — same four amino acid substitutions, same receptor — with one additional chemical group: a maleimidopropionic acid (MPA) linker that covalently binds free serum albumin after injection. The albumin conjugation extends the plasma half-life from ~30 minutes to approximately 8 days. But it also transforms the pharmacologic signal: instead of a pulsatile GH release, the drug produces a sustained flat elevation. Not a stronger pulse — a fundamentally different drug.

A synthetic pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) that binds the ghrelin receptor GHSR-1a on pituitary somatotrophs and hypothalamic neurons, triggering GH release through a pathway parallel and additive to GHRH. Distinguished from older GH-releasing peptides (GHRP-2, GHRP-6) by selectivity: at doses producing GH release, ipamorelin does not activate the ACTH/cortisol or prolactin axes. Research-only; no FDA or EMA approval.

Kisspeptins are endogenous peptides produced by the KISS1 gene and cleaved into several bioactive forms (kisspeptin-54, -14, -13, -10). All share the C-terminal decapeptide (kisspeptin-10) that binds KISS1R (GPR54), a G-protein-coupled receptor expressed on GnRH neurones of the hypothalamic arcuate nucleus. Activation of KISS1R triggers pulsatile GnRH release, which in turn drives LH and FSH secretion from the pituitary. Kisspeptin is now understood to be the primary upstream regulator of the entire hypothalamic-pituitary-gonadal axis; loss-of-function mutations in KISS1R cause hypogonadotropic hypogonadism, and the peptide has been studied in humans by the Dhillo group and others as a physiological substitute for GnRH in hypothalamic amenorrhoea and in assisted-reproduction protocols. There is no approved kisspeptin therapeutic; the compound remains in the investigational phase.

A synthetic cyclic heptapeptide α-MSH analogue with broad activity across all four peripheral melanocortin receptor subtypes: MC1R (skin darkening via eumelanin), MC3R and MC4R (central sexual-response circuitry and appetite regulation) and MC5R (sebaceous / exocrine gland activity). It has never been approved by any regulator. It circulates as a grey-market cosmetic tanning and sexual-response peptide via research-supply channels, and multiple national regulators — including the UK MHRA, Norwegian Medicines Agency, Irish HPRA, and Australian TGA — have issued specific warnings against its cosmetic use. Its historical significance is as the research tool whose accidental sexual-response observation launched the Palatin bremelanotide programme.

A cyclic heptapeptide melanocortin receptor agonist. It acts predominantly at the melanocortin-4 receptor (MC4R) in the central nervous system, with weaker activity at MC1R, MC3R and MC5R. The MC4R-expressing hypothalamic neurones it engages are part of the central sexual-response circuitry — the same neural nodes implicated in appetitive sexual desire. The molecule is bremelanotide, marketed as Vyleesi by AMAG Pharmaceuticals (originally licensed from Palatin Technologies), and FDA-approved on 2019-06-21 for hypoactive sexual desire disorder (HSDD) in premenopausal women as a 1.75 mg subcutaneous injection given on demand roughly 45 minutes before anticipated sexual activity.

The shortest peptide analogue of endogenous growth hormone-releasing hormone (GHRH), consisting of amino acids 1–29 with a C-terminal amide. Binds the pituitary GHRH receptor and stimulates a short, sharp physiologic GH pulse. Historically approved by the FDA as Geref for pediatric GH deficiency in 1990; the NDA was withdrawn in 2008 for commercial reasons. Modern use is exclusively via compounding pharmacies; there is no currently marketed FDA-approved product.