Peptide Library

Proposed to compete with SNAP-25 in the "SNARE" complex, slightly reducing acetylcholine release at the nerve–muscle junction and so softening expression lines — a very mild, reversible version of what botulinum toxin does, if it penetrates…

Blocks nicotinic acetylcholine receptors on adrenaline-releasing cells, so less catecholamine is released; also lowers blood pressure, calms the heart, improves insulin signalling and kills some microbes in animal and cell studies

Activates the kisspeptin receptor (KISS1R, formerly GPR54) on hypothalamic GnRH neurons, which releases GnRH and therefore LH and FSH from the pituitary

Initially stimulates, then desensitises pituitary GnRH receptors, shutting down LH/FSH and so testosterone or oestrogen to castrate/post-menopausal levels within 2–4 weeks

After an initial surge, continuously occupies pituitary GnRH receptors and desensitises them, suppressing LH/FSH and so testosterone or oestrogen to castrate/post-menopausal levels

Competitively blocks pituitary GnRH receptors, so LH and FSH fall within hours, with no initial flare and rapid reversal when stopped

Competitively blocks pituitary GnRH receptors, suppressing LH (and to a lesser extent FSH) within hours, without flare, reversible within 1–2 days of stopping

Selectively activates vasopressin V2 receptors: in the kidney this concentrates urine and retains water; in blood vessels it releases stored von Willebrand factor and factor VIII

Activates V1a receptors (blood-vessel constriction, brain social circuits), V1b receptors (pituitary ACTH release) and V2 receptors (water retention in the kidney, vWF release)

After a brief stimulation, desensitises pituitary GnRH receptors and suppresses LH/FSH, taking oestrogen (or testosterone) to post-menopausal/prepubertal levels

Activates melanocortin receptors MC1R (skin pigmentation, anti-inflammatory), MC3R and MC4R (appetite, energy balance, sexual function) and MC5R (sebaceous and exocrine glands)

The body's own ligand for the growth hormone secretagogue receptor (GHS-R1a): triggers GH release from the pituitary, stimulates appetite via the hypothalamus, speeds stomach emptying and raises blood glucose by restraining insulin

TRH tells the pituitary to release TSH (and prolactin); in the brain it acts as a neuromodulator that increases arousal, motor activity and cerebellar output — taltirelin was built to exploit the brain effects with minimal thyroid effect

Activates somatostatin receptors (mainly SSTR2, also SSTR5) to switch off secretion of growth hormone, many gut hormones and tumour peptides, and to slow gut motility and splanchnic blood flow

Activates somatostatin receptors SSTR2 and SSTR5 to suppress growth hormone and gut/tumour hormone secretion and to slow neuroendocrine tumour growth

Activates four of the five somatostatin receptors (SSTR1, 2, 3 and especially SSTR5) to suppress ACTH from pituitary corticotroph tumours and GH from somatotroph tumours that respond poorly to octreotide or lanreotide

Acts at five receptors (SSTR1–5) to inhibit secretion almost universally — growth hormone, TSH, insulin, glucagon, gastrin and pancreatic enzymes — and to reduce splanchnic blood flow

Binds pituitary GnRH receptors far more durably than natural GnRH; a brief surge of LH/FSH is followed by receptor desensitisation and a sustained shutdown of testosterone or oestrogen production

Continuous GnRH-receptor stimulation desensitises the pituitary, shutting down LH/FSH and therefore testosterone or oestrogen production after an initial flare

Continuous low-level GnRH-receptor stimulation from a hydrogel reservoir desensitises the pituitary and suppresses LH, FSH and sex steroids for a full year

Blocks pituitary GnRH receptors directly, so LH, FSH and testosterone fall within days with no initial surge

Activates uterine oxytocin receptors like oxytocin but resists breakdown, so a single dose keeps the uterus contracted for an hour or more after delivery

Blocks oxytocin from binding its receptor on uterine muscle, lowering intracellular calcium and reducing contraction frequency

CRH stimulates pituitary corticotrophs to release ACTH; ACTH(1-24) stimulates the adrenal cortex (MC2 receptor) to release cortisol — each is used to test the next link in the chain