Kisspeptin peptides have transitioned from agents discovered as metastasis-suppressors to leading players in reproductive neuroendocrinology, as they alone offer a pharmacological "master key" for control of the GnRH "master switch". By activating KISS1R with nanomolar specificity, kisspeptins integrate pubertal timing, ovulatory cyclicity, spermatogenesis, and sexual motivation. Additionally, a growing database links kisspeptins to mood, metabolism, and tissue-specific tumor suppression. The sections that follow will attempt to integrate mechanistic understanding, translational value, and head-to-head comparisons with more widely known peptides so that readers may determine where kisspeptin stands among the ever-growing armamentarium of fertility, hypogonadism and sexual dysfunction therapeutics.
Kisspeptin is a group of amidated peptides characterized by a C-terminal decapeptide which can activate the previously orphan G-protein-coupled receptor that has been variously referred to as KISS1R, GPR54 or AXOR12. Initially discovered as a metastasis suppressor for melanoma, the product of the KISS1 gene is post-translationally processed into shorter peptides that now appear to form part of a biochemical language in which hypothalamic neurons speak to the anterior pituitary. Peptides are synthesized mainly in the infundibular (arcuate) nucleus and the anteroventral periventricular nucleus, however their target receptor is more widely expressed throughout the brain and periphery including in limbic, vascular and pancreatic regions. This wide-spread distribution suggests that kisspeptin may function less as a singular hormone and more as a part of a symphonic cue that influences pulsatility, plasticity and metabolic tempo.
Fig. 1 Kisspeptin/KISS1R signalings.1,2
In the whole vertebrate lineage, the kisspeptin system predates the radiation of the jawed vertebrates, and therefore its reproductive primacy would have been evolved before the Cambrian radiation of the gnathostomes. Cyclostomes, which radiated before the hypothalamic GnRH, already used a kisspeptin-like peptide to regulate seasonal gonad growth in response to water temperature and day length. In contrast, the "updated" role of kisspeptin as a seasonal trigger in modern teleosts (salmon) is, as in many other vertebrates, to up-regulate hypothalamic kisspeptin expression during spring rains, in order to "permit" the migration upstream of early-stage fish to waters of lower salinity, where they continue their growth and gametogenesis. The peptide can therefore be seen as a rheological sensor (receptor) that triggers the release of a neuroendocrine "visa" for gonadal recrudescence. In amphibians, an interesting story is also told. In anuran species that live in variable and unpredictable monsoonal environments, larval density and the risk of pond drying affect kisspeptinergic tone in the magnocellular preoptic nucleus. In the event that the metamorphic climax occurs during a drought, a rapid drop in kisspeptin mRNA levels leads to delayed differentiation of the gonads until the tadpole has found a safe, land-based habitat. It is an example of how the peptide does not just "schedule" reproduction but, in many cases, "dictates" the entire life-history of the individual, by preventing sexual maturation from occurring until somatic and ecological conditions are satisfactory. The reptile lineage has added another element to the kisspeptin picture by subordinating the thermosensitive differentiation of the gonads to kisspeptin tone. In many turtles, high incubation temperatures cause increased hypothalamic kisspeptin expression in males, thus promoting testicular organization, while low temperatures have the opposite effect, and favor ovarian differentiation.
Kisspeptin is encoded by a 145-amino acid prepro-peptide with an N-terminal hydrophobic leader sequence that tethers the nascent protein to the rough endoplasmic reticulum. However, this unremarkable mode of intracellular trafficking is in fact highly dependent on endoplasmic reticulum oxidoreductin; in chronically inflamed hypothalamic neurons, swollen ER cisternae impair cleavage of the leader sequence, and thus reduce the available substrate for further processing. Therefore, even before transcription of kisspeptin mRNA can be modulated, the synthesis of bioactive hormone is already susceptible to proteostatic insults. After leader sequence cleavage, the pro-peptide is trafficked through the Golgi where serine-rich regions are O-glycosylated. The attached glycans thus act as zip codes that determine whether the vesicle fuses to the constitutive or regulated secretory pathway. In a state of leptin sufficiency, O-glycosylation is increased, skewing vesicle sorting towards dense-core granules that release in a stimulus-coupled manner. By contrast, glucocorticoids ablate glycan chains, thereby re-routing kisspeptin towards constitutive secretion that is not activity-dependent. In this way, post-translational sorting can explain how stress can subvert reproductive function in the absence of any gross defects in gene transcription. In the mature granule, pro-hormone convertases PC1/3 and PC2 cleave the bioactive fragments at a pair of basic residues. However, the rate of this cleavage is in turn influenced by luminal pH. Granule acidification is achieved by V-ATPase complexes, the formation of which is enhanced by insulin action through phosphoinositide 3-kinase. Therefore, during insulin deficiency (whether fasting or diabetic), granular pH increases, slow convertase activity and immature intermediates tend to accumulate. Partially processed peptides lack the C-terminal amidation required for high-affinity binding to their receptor, and so can act as competitive antagonists. The peptide synthesis machinery is thus also a metabolic rheostat that gates kisspeptin release.
KISS1R is part of the rhodopsin-like GPCR superfamily, but its intracellular loops contain an unusual enrichment of negatively charged residues that act as an electrostatic Velcro for multivalent signaling scaffolds. The agonist-bound receptor undergoes a conformational change in which transmembrane helix 6 swings outward, creating a cationic groove that becomes an anchoring site for phosphoinositide-dependent kinase-1 in a manner that bypasses classical G-protein coupling. This noncanonical pathway phosphorylates AKT at threonine 308 and promotes neuronal survival under conditions of excitotoxic glutamate challenge. The receptor does not simply relay a reproductive impulse; it also brokers a neuroprotective pact, and this is to say that signaling is never monophonic. The bifurcation of signaling cascades downstream of Gαq and the hydrolysis of PIP2 by phospholipase Cβ is a textbook example, which generates diacylglycerol and IP3. In high-density cultures of GnRH neurons, diacylglycerol engages protein kinase Cε, which translocates to the nucleus and activates the Gnrh1 promoter through the de-repression of repressive histone methylation marks. In low-density cultures, however, diacylglycerol is more readily metabolized by diacylglycerol kinases to form phosphatidic acid, which can then be used as a source of membrane expansion to support the GnRH neuron's dendritic arborization. So the same biochemical precursor has a transcriptional or a morphogenic fate depending on the social environment of the neuron, which is to say that receptor logic is also a matter of micro-environmental semantics. The receptor also couples to Gαs when chronically exposed to its agonist and steers adenylyl cyclase towards weak cAMP oscillations that preferentially activate exchange proteins activated by cAMP (Epac) instead of protein kinase A. Epac-Rap1 signaling increases gap-junctional coupling between GnRH cell bodies and so synchronizes their pulsatile activity. This rewiring helps to explain why pulsatile kisspeptin administration can preserve LH rhythmicity even as continuous kisspeptin infusions ultimately attenuate it: the receptor itself is performing a temporal alchemy, transmuting an unceasing ligand flux into a metronomic cAMP wave that enforces network coherence. These are emergent properties that cannot be foreseen from the kinetics of ligand binding alone. They are the products of a recursive dialogue between receptor conformation and cellular choreography.
Instead of trying to list individual clinical endpoints, it may be more useful to view kisspeptin as a discourse through which the hypothalamus is arbitrating various 'stories' of energy deficit, inflammatory insult, circadian timing and sexual arousal. The clinical advantages may then be the reestablishment of a dialogue through silenced neuroendocrine pathways resulting from constitutional, functional or drug-induced injury.
Activation of quiescent GnRH neurons by kisspeptin is not the result of a simple pharmacological reboot. Rather, it is the result of a de-escalated, and developmentally recapitulated, sequence of events. Kisspeptin, once again, allows the episodic Ca2+ signal which fetal GnRH neurons use to prime the pituitary for reproductive destiny to be brought online in the adult. In conditions such as functional hypothalamic amenorrhoea, the 'fetal language' of GnRH neuronal communication with the pituitary is repressed by metabolic and psychosocial stressors. Kisspeptin treatment, therefore, is re-teaching an ancient, GnRH neuronal arcuate dialect once more. It does so without creating the supraphysiological drive of hormone replacement therapy with gonadotropins. In addition to reactivating GnRH neurons, chronic kisspeptin also reinstates dendritic spines (carrying NMDA receptors) on GnRH neurons that had been lost in the extended quiescent state. This kisspeptin-promoted spine growth allows GnRH neurons to remain susceptible to excitatory glutamatergic inputs from hypothalamic circadian and metabolic centers, which allows the GnRH pulse generator to be reintegrated into the neuroendocrine 'neural network' and prevents an over-autonomous reproductive axis which could be more vulnerable to reproductive disorders in the future. Kisspeptin, therefore, allows for immediate reactivation and future-proofing.
Within the antral follicle, kisspeptin is concentrated in the mural granulosa layer immediately adjacent to the basal lamina and therefore well placed to interact with thecal vasculature. There, kisspeptin inhibits the transcriptional magnitude of vascular endothelial growth factor-A by preventing the recruitment of hypoxia-inducible factor-1α to the VEGF-A promoter. This dampened angiogenesis inhibits the leakiness of the developing capillaries and thereby averts the ovarian hyper-stimulation syndrome. The reduction in capillary leakiness is however more a softening than an abolition: follicles do still receive a wreath of vascularization sufficient to supply steroidogenic substrates, but they are less "plasma leaky" and do not promote a plasma-leaky vasculopathy that can induce third-spacing of fluids. Kisspeptin, by softening angiogenic expression, is in essence editing out the descriptive adjectives in the angiogenic description without tampering with the basic message. In addition to this effect, kisspeptin modulates the biomechanics of the cumulus oophorus. Kisspeptin down-regulates some matrix metalloproteinases while up-regulating their tissue inhibitors, thereby increasing the viscoelasticity of the extracellular matrix that surrounds the oocyte and the accompanying cumulus mass. This resistance to shear stress allows the oocyte to be extruded in a cohesive cumulus ball, improving its entrapment by the fimbrial ostium and the chance of ectopic ovulation that can seed endometriotic lesions. Kisspeptin, therefore, confers a biomechanical finesse as well as endocrine benefits.
In the interstitium of the testis, Leydig cells display KISS1R at a neuronal density and frequency. Intratesticular pulsatile administration of kisspeptin recapitulates the staccato pulses of dihydrotestosterone that drive progression of the spermatogonia through the blood–testis barrier. These pulses are also maintained within a physiological range that stabilizes the Sertoli-cell tight-junctional proteome that supports the immune privilege that protects against the development of antisperm antibodies. The peptide thus facilitates a local androgenic code that is both legible to the germ cells but opaque to the general circulation, and thus does not induce the erythrocytogenic and dermatogenic consequences associated with systemic administration of testosterone. Kisspeptin also seems to modulate peritubular myofibroblast contractility that drives sperm into the rete testis. Regulation of endothelin-1 sensitivity by the peptide avoids hypercontractile states that would otherwise lead to tubular sludging and focal ischemia. The clinical benefit is a qualitatively improved ejaculate with reduced reactive oxygen species and improved sperm membrane integrity as well as count.
Kisspeptin, the interpreter of energy, clock and gonadal signals for GnRH neurons, has multiple and context-dependent functions, from activation of puberty to subtle regulation of fertility in adults. It also links metabolism with reproductive function and is involved in the switch between slow and fast metabolisms during pregnancy. Kisspeptin is not a simple reproductive on–off switch, but rather a metabolic and reproductive rhetorical negotiator of the GnRH neuron environment.
In the pre-pubertal period, the GnRH neuronal network is a soft-spoken one. The GnRH voice coach, kisspeptin, can induce the necessary pulsatile oratory of this group for sexual maturation. In the pre-pubertal dormant period, repressors of transcription (i.e. GABAergic and neuropeptide Y signaling) keep chromatin in a state that silences kisspeptin gene expression. Upon somatic growth nearing a metabolic set point, leptin and insulin alter epigenetics to permit the recitation of the kisspeptin script. Kisspeptin then binds KISS1R on GnRH perikarya and evokes oscillatory calcium waves which co-ordinate the entire neuronal ensemble. This shift is not just a hormone-mediated event; rather, it is a narratological one as well in which the pre-pubertal lullaby is transformed into the adolescent ballad of rising sex steroids.
In the adult animal, kisspeptin neurons in the arcuate nucleus act as the metronome for LH pulsatility; those in the anteroventral periventricular nucleus drive the pre-ovulatory surge. The two systems talk different languages: arcuate kisspeptin is under sex-steroid negative feedback; the periventricular group is sensitive to oestradiol positive feedback. The use of this single peptide to express both tonic and cyclic information reflects a fundamental narrative constraint, providing a mechanism for gametogenesis to be tightly linked in synchrony with the ovary or testis. The advantage is a common language that can be understood across variable metabolic and emotional states.
The kisspeptin neuron is rich in receptors for leptin, insulin, and glucocorticoids. Kisspeptin neurons can thus be described as polyglot in the language of metabolism. During negative energy balance, low leptin and high cortisol signal to the kisspeptin promoter to repress transcription. Inflammatory cytokines also activate microglia to release prostaglandins which desensitize kisspeptin secretion, thereby coordinating stress from the immune system with reproductive silence. As a biosynthetic babel fish, kisspeptin ensures that the reproductive axis fires only when the somatic, immune, and emotional languages are in agreement.
Kisspeptin, by activating its specific G-protein-coupled receptor, KISS1R, can modulate a number of intracellular signalling pathways. These changes can lead to alterations in neuronal electrical activity, synaptic structure and glial communication. This is a bidirectional process as the same ligand–receptor pair can activate different signalling cascades depending on the cellular environment, temporal dynamics and metabolic state. The resulting physiological response can be both local and widespread, short and long-term.
Binding of KISS1R heterodimerises it with a preference for Gαq/11. This coupling results in the activation of phospholipase Cβ, which cleaves PIP2 to produce diacylglycerol and IP3. IP3 then induces the release of Ca2+ from endoplasmic stores and diacylglycerol activates protein kinase C isoforms which go on to phosphorylate voltage gated ion channels. In GnRH neurons this results in the inhibition of inwardly rectifying K⁺ currents and the recruitment of a non-selective cation conductance. These two effects produce a slow depolarization which sums with pacemaker oscillations, eventually generating an electrical crescendo. However, this signal is not simply additive, as it entrains silent neurons to the pacemaker oscillations, a phenomenon that demonstrates that the predominant language of kisspeptin is electrical rather than chemical.
In addition to the rapid excitation of GnRH neurons, repeated kisspeptin stimulation leads to the generation of new dendritic spines, in a CaMKII-dependent mechanism that involves the reorganization of the actin cytoskeleton. The newly generated spines are enriched in NMDA receptors, which increases the sensitivity of GnRH neurons to glutamatergic signals from the circadian and metabolic centers. The increase of dendritic spines can be rapidly reversed by the removal of kisspeptin stimulation, which leads to dendritic spine retraction and pruning. This plasticity in the GnRH neurons translates into a 'use-it-or-lose-it' principle for reproductive capability.
KISS1R is also expressed in astrocytes which, when stimulated by kisspeptin, release the diffusible signal prostaglandin E2 (PGE2). PGE2 in turn has a direct effect on the excitability of GnRH neurons. This tripartite conversation adds a layer of glial fine-tuning to amplify or constrain the peptidergic signal. Astrocytic kisspeptin signalling is attenuated by metabolic stress, and the resulting PGE2 release is unchecked, leading to a disruption of LH pulsatility. This mechanism shows that kisspeptin mode of action is not restricted to neuronal membranes, but also takes place in the astroglial reticulum that pervades the hypothalamus, and the local metabolic gossip is translated into global reproductive outcomes.
Kisspeptin and PT-141 are distinct investigational peptides used for different purposes in sexual-health research. Kisspeptin is the principal central regulator of the reproductive system: it depolarizes GnRH neurons in the hypothalamus via Kiss1R to restore physiological pulsatile secretion of LH and FSH, which in turn drives gonadal steroidogenesis, gametogenesis and the associated neuro-endocrine milieu that supports libido and fertility. In this sense, its effects are both hierarchical (i.e. upstream of gonadal steroidogenesis), and dependent on downstream end-organs; they are also accumulative, as benefits may take time to manifest while the full hormonal axis gradually re-awakens. Kisspeptin is therefore appropriate for disorders of hypogonadotropic hypogonadism, functional amenorrhoea or sub-fertility where re-establishment of physiologic rhythm is the goal. In contrast, PT-141 (bremelanotide) circumvents the HPG axis completely, being a melanocortin-4 receptor agonist in limbic and hypothalamic centers which serve arousal, reward and autonomic tone. The resultant pro-libido effect is fast, hormone-independent and largely limited to motivational aspects of sexual behavior; gonadotropin or steroid levels are not affected, and gametogenic or ovulatory effects are neither expected nor reported. For this reason, PT-141 is being studied for on-demand acute enhancement of desire—most often in premenopausal women with hypoactive sexual desire disorder, or in men whose erectile difficulties remain despite preserved vascular status—while kisspeptin is being researched for the chronic restoration of reproductive endocrine function. Their side-effect profiles are also in many ways divergent: kisspeptin shares the liabilities of the gonadal steroids it induces (such as oestrogen-dependent mood swings and androgen-mediated sebum production), while PT-141 can cause transient nausea, flushing and mild BP increases as a result of melanocortin receptor activation outside the brain. The two molecules are thus ultimately complementary rather than interchangeable: kisspeptin recapitulates the natural hormonal choreography that licences sexual activity, while PT-141 provides a fast, central arousal cue that is endocrine-independent. Combined regimens—low-dose kisspeptin to support a eugonadal background with intermittent PT-141 to boost motivational drive—are a possibility, although specific pharmacokinetic and safety interaction data are as yet unavailable.
Want to know more about pt141, see this article What is PT-141?
Gonadorelin (synthetic GnRH) and kisspeptin both stimulate the HPG axis, but in very different places and with different pharmacodynamics. Gonadorelin is a synthetic decapeptide identical to endogenous GnRH; it acts directly on GnRH receptors in the anterior pituitary gland to elicit a fast response, with no role for the hypothalamus. As the peptide is rapidly degraded, pulsatile administration with an electronic pump is essential to reproduce physiologic interpulse periods; continuous administration causes down-regulation of the GnRH receptor and decreases gonadotropin levels (useful therapeutically for prostate cancer or endometriosis, but not wanted when fertility is desired). Kisspeptin works on GnRH neurones at the hypothalamic level that actually controls GnRH release: in this way, it elicits the release of endogenous GnRH, and in a hypothalamic-dependent way acquires its own inherent rhythm-generating system. The difference in synaptic level gives kisspeptin two practical advantages. First, LH/FSH release is inherently pulsatile, so that no pumps are required, and desensitization to treatment is avoided. Second, the rise in sex steroids is more physiologic, moderated by the hypothalamus and preserving the capacity to make oestradiol or testosterone, and therefore preserving the spermatogenic or folliculogenic capacity of the gonads. On the other hand, kisspeptin has a much shorter half-life in the circulation, requiring multiple daily injections or intranasal administration, and is less potent if GnRH neurones are missing or are desensitized. In studies of congenital hypogonadotropic hypogonadism, pulsatile gonadorelin therapy leads to an earlier return of spermatogenesis compared to exogenous gonadotropins, and kisspeptin causes an increase in gonadotropins to the mid-normal range, but at a slower rate. Safety and tolerability also differ: gonadorelin is associated with complaints related to acute, pharmacological stimulation of the gonadotropins (swelling of the gonads, surge flu), whereas the problems with kisspeptin are mostly local reactions to injection and transient facial redness. Gonadorelin is approved in some countries for some protocols of ovulation induction and treatment of hypogonadism, while kisspeptin remains an investigational medicine. In summary, gonadorelin is a fast-acting direct pituitary stimulator but requires a pump and can lead to desensitization, whereas kisspeptin is an indirect, slower, but self-modulating and physiologic GnRH releaser that is still developing its dosing schedule and delivery methods.
As of the latest available information, kisspeptin or any of its derivatives do not hold a full marketing authorization as an independent medicinal product by the United States Food and Drug Administration. It is an investigational peptide that can only be administered to human subjects as part of clinical protocols which have undergone Agency review, or, under highly limited conditions, as a bulk substance for compounding that is itself a subject of active regulatory review. The Agency has, on several occasions, expressed a scientific interest in the molecule, convening advisory panels and providing briefing documents on its alleged benefits versus poorly understood safety concerns.
The observed t1/2 for kisspeptin-10 is the result of a "symphony" of biochemical and physical processes that is initiated as soon as the peptide is ejected from the syringe. Bloodborne aminopeptidases, including membrane-associated (CD13) and cytosolic forms of alanyl- and leucyl-aminopeptidase, hydrolyze the N-terminal Tyr1-Asn2 linkage with catalytic efficiency (KM, kcat) similar to what has been reported for angiotensin metabolism; as the product of this cleavage is not a substrate for KISS1R, this step is essentially irreversible. Separately, the low molecular weight (~1.3 kDa) supports rapid glomerular filtration and kisspeptin-10 appears in the urine within 2 minutes of IV administration. Tubular reabsorption is limited due to the linear, hydrophilic character of the sequence (i.e., no bulky aromatic moieties for megalin/cubilin endocytic receptors); hence the kidney acts as an effective "sink" to prevent peripheral accumulation. Efforts to extend this exposure followed two non-mutagenic approaches. One approach is competitive enzyme inhibition: infusion of bestatin or diprotin A (dipeptidyl-peptidase IV inhibitors) retards the initial cleavage and prolongs the terminal phase into the 15–20 min range with no change to receptor kinetics. A second approach is formulation physics: loading into 80-nm PEGylated liposomes forms a depot that slowly releases peptide into the extravascular space, resulting in measurable plasma levels for up to 4 hours with no modification to the native sequence that is required for regulatory acceptance. Microdialysis studies in rat hypothalamus show that even very brief arterial pulses can trigger prolonged electrical bursts in GnRH neurons because intracellular Ca²⁺ waves persist long after the agonist has been cleared; this time decoupling means that ultra-short t1/2 is not a limitation for physiological stimulation per se but a safety mechanism to avoid receptor desensitization. Investigators designing dynamic test protocols should therefore consider "effective" half-life at the receptor level—driven by second-messenger decay—rather than rely solely on pharmacokinetic tables when determining timing of repeated boluses.
Kisspeptin is is an endogenous regulator of the HPG axis. Kisspeptin appears to be the critical physiological regulator of the HPG axis and mediates a broad range of input signals from metabolism, circadian timing, and stress to regulate the pulsatile release of gonadotropin-releasing hormone. In numerous studies, kisspeptin has been shown to cause pulsatile release of LH and FSH in functional hypothalamic amenorrhoea, congenital hypogonadotropic hypogonadism, and iatrogenic suppression, to restore ovarian or testicular function. Kisspeptin does not cause supraphysiological peaks of steroids as do exogenous gonadotropins. The shorter bioactive fragment, kisspeptin-10, has a short elimination half-life of approximately 6 minutes, a pharmacokinetic limitation that has so far necessitated the use of a continuous infusion or administration in closely spaced boluses. Kisspeptin and the melanocortin-4 agonist PT 141 have been found to have mutually orthogonal mechanisms of action; kisspeptin re-establishes the neuroendocrine basis of fertility, whereas PT 141 induces a rapid sexual arousal through a brain-based mechanism that does not involve the reproductive hormone cascade. In another comparison with GnRH, the GnRH analogue gonadorelin, kisspeptin provides more physiological and self-limiting stimulation of the gonadotropes.
Kisspeptin Peptides We Provides
| CAT# | Product Name | M.W | Molecular Formula | Inquiry |
|---|---|---|---|---|
| K04001 | Kisspeptin-13 (4-13) (human) | 1302.46 | C63H83N17O14 | Inquiry |
| K04002 | Kisspeptin-54 (human) | 5857.51 | C258H401N79O78 | Inquiry |
| K04003 | Kisspeptin-54 (27-54) (human) | 3229.69 | C149H226N42O39 | Inquiry |
| K04004 | Kisspeptin-13 (human) | 1626.84 | C78H107N21O18 | Inquiry |
| M04006 | Kisspeptin-10 Metastin (45-54), Human | C63H83N17O14 | Inquiry | |
| M04007 | Kisspeptin-13 | C78H107N21O18 | Inquiry | |
| M13002 | Kisspeptin-14 | Inquiry | ||
| M13006 | Kisspeptin-10_mouse | Inquiry | ||
| R0925 | Kisspeptin 10 (dog) | 1330.51 | C65H87N17O14 | Inquiry |
| R0938 | Kisspeptin 234 | 1295.4 | C63H78N18O13 | Inquiry |
| R1469 | Kisspeptin-10 | 1302.4 | C63H83N17O14 | Inquiry |
| R1470 | Kisspeptin-10 Trifluoroacetate | 1416.46 | C63H83N17O14.C2HF3O2 | Inquiry |
| R2281 | Kisspeptin-10, rat | 1318.4 | C63H83N17O15 | Inquiry |
| R2438 | Kisspeptins | 5857 | C258H401N79O78 | Inquiry |
| R2372 | Kisspeptin-54 (27-54) (human) trifluoroacetate salt | 3229.6 | C149H226N42O39 | Inquiry |
References
