Benefits from structured on/off cycles for sustained response. See dosing section.
Ipamorelin arrived from Novo Nordisk research in the late 1990s as an answer to a specific pharmacological problem: how do you selectively stimulate GH secretion from the pituitary without triggering the cortisol, prolactin, and ACTH release that characterized earlier GHRPs? The answer was a rationally designed pentapeptide — five amino acids, one of which is a non-natural building block (2-aminoisobutyric acid, Aib), another a D-stereoisomer naphthylalanine. These structural choices were not arbitrary: they emerged from systematic structure-activity relationship work to retain ghrelin receptor (GHSR-1a) binding affinity while eliminating the off-target pituitary interactions that compromised GHRP-6 and hexarelin’s research utility. The 1998 Raun et al. publication (PMID 9849822) in the European Journal of Endocrinology formally established what that optimization achieved: ipamorelin was, in the authors’ words, “the first selective growth hormone secretagogue” — an explicit claim validated by head-to-head comparisons with GHRP-6 and GHRP-2. What makes this selectivity matter in research practice is more than a cleaner side effect profile. Cortisol and GH are physiologically antagonistic — cortisol suppresses GH-mediated anabolism, increases insulin resistance, and promotes visceral fat accumulation. A GHRP that simultaneously elevates both hormones is working against itself for body composition and recovery endpoints. Ipamorelin sidesteps this by activating GHSR-1a without the secondary ACTH/CRH pathway stimulation. The result is a GH pulse that can actually drive the metabolic effects researchers are investigating — without a concurrent cortisol signal blunting them. This is not a marginal distinction: in protocols targeting body composition, fat loss, muscle preservation, and recovery, the selectivity difference between ipamorelin and GHRP-6 is mechanistically significant. The combination with CJC-1295 No DAC (Modified GRF 1-29) transforms ipamorelin from a useful standalone into what compounding clinic consensus consistently describes as the most rational dual-receptor GH secretagogue protocol. GHRH receptor activation (via CJC-1295 No DAC) and ghrelin receptor activation (via ipamorelin) converge on two independent intracellular signaling pathways in pituitary somatotrophs: Gs/cAMP via GHRHR, and Gq/IP3-DAG via GHSR-1a. The simultaneous activation of both pathways produces a GH pulse substantially greater than either compound alone — the pharmacological basis of the stack. The simultaneous administration timing is critical: both compounds must be injected at the same time to capture the synergistic window before the GHRH receptor signal decays. From a research design perspective, ipamorelin occupies a unique position in the GHRP class: it is the compound that most closely isolates the GH axis effect for study, because it produces the smallest confounding footprint on other hormonal systems. This is the property that makes it scientifically preferred for protocols where researchers want to study GH, IGF-1, body composition, sleep, or recovery without the cortisol and appetite variables that other GHRPs introduce. For practitioners building research protocols in compounding clinic settings, ipamorelin’s combination of validated Phase I/II human data, established selectivity, and synergistic activity with CJC-1295 No DAC makes it the default GHRP selection in the absence of specific contraindications.
Researchers studying growth hormone optimization without the cortisol and prolactin side effects associated with GHRP-6 and hexarelin — ipamorelin’s published selectivity profile makes it the preferred GHRP in protocols where GH stimulation is the exclusive research endpoint.,Populations investigating body composition improvements — pulsatile GH stimulation drives visceral lipolysis, lean mass preservation, and IGF-1-mediated anabolism without the glucocorticoid interference that broader-spectrum GHRPs introduce.,Sleep quality and nocturnal recovery research — ipamorelin’s pre-bed dosing protocol targets the peak GH secretory window during slow-wave sleep onset, amplifying the endogenous nocturnal GH pulse without disrupting sleep architecture.,Research subjects studying the synergistic GHRH + GHRP combination protocol — ipamorelin is the near-universal GHRP component in CJC-1295 No DAC stack designs due to its favorable selectivity and well-characterized dose-response curve.,Long-duration research protocols where cumulative ACTH and cortisol exposure is a confounding concern — ipamorelin’s selectivity allows extended protocol durations without the HPA axis activation that limits GHRP-6 and hexarelin use cases.
Ipamorelin is a synthetic pentapeptide ghrelin receptor (GHSR-1a) agonist. Its sequence — Aib-His-D-2-Nal-D-Phe-Lys-NH2 — was rationally designed to bind GHSR-1a with high affinity while avoiding the structural motifs that drive off-target pituitary receptor activity in earlier GHRPs. The N-terminal Aib (2-aminoisobutyric acid) is a non-natural alpha-methyl amino acid that confers resistance to aminopeptidase cleavage while adopting a helix-inducing conformation. The D-2-Nal (D-naphthylalanine) at position 3 provides the hydrophobic contact critical for GHSR-1a binding — a pharmacophore feature shared across the GHRP class, but positioned with different flanking residues in ipamorelin to achieve the selectivity profile. Upon binding GHSR-1a on pituitary somatotroph cells, ipamorelin activates the Gq protein-coupled signaling cascade: Gq → phospholipase C (PLC) activation → inositol 1,4,5-trisphosphate (IP3) + diacylglycerol (DAG) → IP3-driven Ca2+ release from endoplasmic reticulum + DAG-driven protein kinase C (PKC) activation → convergent Ca2+ elevation → GH-containing secretory vesicle exocytosis. The Ca2+ signal is also augmented via voltage-gated Ca2+ channel opening. The net result is a discrete GH pulse from the anterior pituitary proportional to receptor occupancy and downstream signal amplitude. Ipamorelin’s selectivity advantage — minimal cortisol, prolactin, and ACTH stimulation at research doses — arises because it does not activate the corticotroph ACTH/CRH pathways or lactotroph prolactin pathways at physiologically relevant concentrations, unlike GHRP-6 and hexarelin (Raun et al., 1998, PMID 9849822). The synergistic amplification with CJC-1295 No DAC (a GHRHR agonist) occurs because GHRHR and GHSR-1a couple to distinct G proteins: GHRHR → Gs → adenylyl cyclase → cAMP ↑ → PKA activation; GHSR-1a → Gq → IP3/DAG/Ca2+ as described above. These two intracellular pathways converge on the same secretory machinery in the somatotroph cell. When both receptors are activated simultaneously, the combined intracellular signal is substantially greater than the sum of either pathway alone — the mechanistic basis of the supra-additive GH pulse documented in human physiology research on GHRH + GHRP combinations. The GH released then acts at peripheral GH receptors to stimulate hepatic IGF-1 synthesis and drive direct lipolytic, anabolic, and tissue repair effects.
Ipamorelin: The First Selective Growth Hormone Secretagogue
Raun K et al. (1998, PMID 9849822) published the foundational characterization of ipamorelin in the European Journal of Endocrinology. This Novo Nordisk study established that ipamorelin stimulates dose-dependent GH release in rats and demonstrated selectivity for GH over ACTH and cortisol — the defining pharmacological property. In comparative studies, ipamorelin stimulated GH release equivalently to GHRP-6 and GHRP-2 while producing significantly less ACTH and cortisol elevation. Phase I dose-escalation data confirmed dose-dependent GH release in human subjects across the 1–100 mcg/kg range. The authors explicitly described ipamorelin as ‘the first selective growth hormone secretagogue’ — a characterization that has held up through subsequent research.
GHRH + GHRP Synergy: Supra-Additive GH Release via Dual-Receptor Activation
Bowers CY et al. (1991, PMID 2827003) established that combined administration of GHRH and a synthetic GHRP (hexapeptide ghrelin-receptor agonist) produces GH release substantially greater than either compound alone — the result of two distinct intracellular signaling pathways (Gs/cAMP via GHRHR and Gq/IP3-DAG via GHSR-1a) converging on somatotroph GH secretion. This synergy is the mechanistic foundation of all GHRH + GHRP combination protocols, including the CJC-1295 No DAC + Ipamorelin stack that represents the compounding clinic consensus standard.
MK-677 (GHSR-1a Agonist) Human Phase II: GH/IGF-1 and Body Composition Effects
Svensson J et al. (1997, PMID 9024227) conducted a 2-month randomized trial of oral MK-677 (ibutamoren), an oral GHSR-1a agonist mechanistically analogous to ipamorelin, in obese subjects. The study documented significant increases in GH secretion, fat-free mass, and energy expenditure compared to placebo. While MK-677 differs pharmacokinetically from ipamorelin (oral, 24-hour duration vs. SubQ, 2-hour half-life), both act through the same GHSR-1a receptor mechanism — making MK-677 human trial data relevant for understanding ipamorelin’s downstream effects. The Svensson study also demonstrated that GH pulse amplitude increases from GHSR-1a stimulation produce measurable fat-free mass gains over a 2-month protocol.
Pulsatile GH Optimization — Body Composition and Lean Mass Research
The foundational research application for ipamorelin is selective GH pulse amplification for body composition studies. When co-administered with CJC-1295 No DAC, ipamorelin provides the GHSR-1a (ghrelin receptor) component of a dual-receptor protocol that produces GH pulses significantly greater than either compound alone. The selectivity profile is critical here: unlike GHRP-6 or hexarelin, ipamorelin does not co-stimulate cortisol or prolactin, which means the GH signal operates without the glucocorticoid interference that would otherwise blunt anabolic and lipolytic endpoints. In body composition research, the GH pulse driven by ipamorelin + CJC-1295 No DAC targets three downstream mechanisms: (1) visceral lipolysis via hormone-sensitive lipase activation, driven by GH-receptor engagement in adipocytes; (2) lean mass preservation via IGF-1-mediated protein synthesis and anti-apoptotic signaling in muscle; and (3) collagen synthesis via IGF-1 effects on connective tissue fibroblasts. The fasted-state dosing requirement is critical: insulin elevation from recent food intake activates somatostatin release, which suppresses pituitary GH secretory response to both GHRHR and GHSR-1a stimulation. All protocol designs require a minimum 2-hour fasted window for full GH response. Phase I/II data from Raun et al. (1998, PMID 9849822) established dose-dependent GH release across a wide dose range. The 100–300 mcg SubQ dose (1.5–4 mcg/kg for an 80 kg subject) falls within the linear portion of the dose-response curve where GH stimulation increases predictably with dose — making it the standard compounding clinic reference range.
Nocturnal GH Pulse Amplification and Sleep Quality Research
The largest GH secretory pulse of the day occurs during the first slow-wave sleep (SWS) episode approximately 60–90 minutes after sleep onset. This pulse is driven by a hypothalamic GHRH surge that activates pituitary GHRHR — and is further amplified by concurrent ghrelin receptor (GHSR-1a) tone from the hypothalamus. Ipamorelin administered 30–60 minutes pre-bed captures this synergistic window: the exogenous GHSR-1a agonist reaches pituitary concentration at the same time the natural GHRH pulse arrives, producing a substantially amplified nocturnal GH peak. The relevance of this nocturnal GH peak for research subjects studying recovery, body composition, and biological aging is significant. GH secreted during SWS drives tissue repair, protein synthesis, collagen production, and anti-catabolic signaling during the most active regenerative window of the day. Age-related decline in SWS-associated GH secretion is one of the best-characterized features of somatotropic aging — beginning in the third decade and accelerating through middle age. Ipamorelin pre-bed dosing is specifically designed to restore amplitude to this declining nocturnal pulse. From a sleep architecture standpoint, ipamorelin’s short half-life (estimated 2 hours) means the pharmacological stimulus is largely cleared before full sleep onset. Unlike long-acting GH secretagogues or exogenous GH, pulsatile GHSR-1a stimulation does not maintain sustained elevated GH levels through the night — preserving the natural GH pulse rhythm that sleep architecture depends on.
Recovery and Tissue Repair Support
GH and IGF-1 are the primary systemic drivers of tissue repair, connective tissue synthesis, and anabolic recovery following exercise or injury. Ipamorelin-driven GH pulses activate hepatic IGF-1 production, which in turn stimulates satellite cell activation in skeletal muscle, collagen synthesis in tendons and ligaments, and protein synthesis pathways across multiple tissue types. Research subjects studying post-exercise recovery, joint health maintenance, or connective tissue integrity find the ipamorelin + CJC-1295 No DAC stack relevant because it addresses the GH/IGF-1 anabolic axis systematically. Compared to direct repair peptides such as BPC-157 or TB-500, ipamorelin operates through a systemic endocrine mechanism rather than local tissue-targeted action. This makes it complementary to — rather than a substitute for — direct repair peptides in recovery protocols. The combination of systemic GH/IGF-1 amplification (via ipamorelin + CJC-1295) and local tissue-directed repair (via BPC-157 or TB-500) addresses recovery through two distinct and non-redundant mechanisms. For research protocols targeting muscle preservation and connective tissue integrity in aging subjects, ipamorelin’s selectivity profile is particularly relevant: the absence of cortisol co-stimulation means the anabolic effects of GH/IGF-1 are not simultaneously opposed by glucocorticoid-mediated protein catabolism and anti-inflammatory signaling.
Anti-Aging and Somatotropic Decline Research
Human GH secretion declines approximately 14% per decade after age 30, driven by increased somatostatin tone, reduced GHRH pulse amplitude, and decreased pituitary GHSR-1a sensitivity. This somatotropic decline correlates with well-documented changes in body composition (visceral fat accumulation, lean mass reduction), bone density, recovery capacity, and sleep architecture. Research protocols studying reversal or attenuation of age-related somatotropic decline represent a growing area of clinical investigation. Ipamorelin’s selectivity profile makes it particularly suited to this research context. Age-related somatotropic decline is not accompanied by equivalent cortisol decline — in fact, HPA axis activity tends to remain elevated or increase with aging while GH secretion falls. A GHRP that co-stimulates cortisol and prolactin would therefore amplify an already-dysregulated endocrine environment. Ipamorelin’s selective GH stimulation without cortisol or prolactin co-activation addresses the specific deficit — declining GH pulse amplitude — without adding to the hormonal imbalance that characterizes somatotropic aging. Compounding clinic consensus for aging-focused GH secretagogue protocols consistently selects ipamorelin as the GHRP component, paired with CJC-1295 No DAC for GHRHR stimulation. The 8–12 week cycle structure with 4-week washout is designed to maintain receptor sensitivity and prevent the desensitization that reduces protocol efficacy over time.
Hypothalamic-Pituitary Axis
Primary site of action. Ipamorelin binds GHSR-1a on pituitary somatotrophs with high affinity, triggering a discrete pulsatile GH secretion event. The hypothalamus modulates baseline GHSR-1a sensitivity via somatostatin and endogenous GHRH tone; ipamorelin’s signal is additive to — not a replacement for — the natural GH secretory rhythm.
Liver / Endocrine
GH released by ipamorelin stimulation binds hepatic GH receptors, driving IGF-1 synthesis and secretion. IGF-1 is the primary anabolic mediator of the GH axis — responsible for protein synthesis, lean tissue maintenance, and collagen production downstream of GH stimulation.
Adipose Tissue / Metabolic
GH drives lipolysis preferentially in visceral adipose tissue via HSL activation. Unlike cortisol (which promotes visceral fat deposition), ipamorelin’s selective GH stimulation — without cortisol co-elevation — targets the visceral fat compartment while supporting lean mass. This selectivity is mechanistically important for body composition research endpoints.
Musculoskeletal / Connective Tissue
GH and IGF-1 stimulate protein synthesis, satellite cell activation in muscle, and type I collagen synthesis in tendons and ligaments. Recovery-focused research protocols targeting the ipamorelin + CJC-1295 stack are designed around this anabolic and repair-promoting axis — particularly via pre-bed dosing aligned with the nocturnal GH pulse.
Central Nervous System / Sleep Architecture
GH secretion is tightly coupled to slow-wave sleep (SWS) onset. Ipamorelin administered pre-bed amplifies the GHSR-1a component of the nocturnal GH pulse, augmenting the endogenous sleep-associated GH secretory event. Improved sleep depth and quality are documented in GH secretagogue research as secondary endpoints.
GH Release / Body Composition / Sleep — paired with CJC-1295 No DAC
Research Rationale
Ipamorelin is one of the most selective GHRPs — stimulates GH release via the ghrelin receptor (GHSR-1a) with minimal cortisol, prolactin, or ACTH side effects, unlike GHRP-6 or hexarelin. Phase I/II clinical trials (Raun K et al., 1998, PMID 9849822) demonstrated dose-dependent GH release at 1–100 mcg/kg. The 100–300 mcg range (equivalent to ~1.5–4 mcg/kg for an 80 kg subject) is the standard compounding clinic reference range, falling within the linear portion of the dose-response curve. Ipamorelin must be injected simultaneously with CJC-1295 No DAC to capture the synergistic dual-receptor GH pulse — sequential administration is suboptimal. First-time researchers should begin at the low end (100 mcg) and assess tolerance before advancing. Source: Pineland dosing.json (Ipamorelin entry, sourceType: clinical_trial), Raun K et al. 1998.
Ipamorelin has a favorable safety profile among GHRP compounds based on published Phase I/II clinical trial data (Raun et al., 1998, PMID 9849822) and extensive compounding clinic use. The defining safety advantage of ipamorelin over other GHRPs is its selectivity: at research doses of 100–300 mcg, ipamorelin does not produce meaningful cortisol or prolactin elevation — effects that limit GHRP-6 and hexarelin use in certain research contexts. ACTH stimulation is also minimal. Known adverse effects consistent with the GHRP/GH class include: mild injection site reactions (redness, transient swelling), flushing at higher doses, transient water retention (via GH-mediated aldosterone effects), and mild fatigue or dizziness in some subjects at first administration. The transient flushing and water retention are typically self-limiting within the first 1–2 weeks of a protocol as the body adapts to increased GH pulsatility. Fasted-state dosing is a safety requirement as well as an efficacy requirement: eating within 2 hours of injection elevates insulin, which activates somatostatin and suppresses GH response — but elevated insulin also modulates the metabolic effects of the resulting GH pulse. Timing discipline is therefore both mechanistically important and metabolically relevant. Regulatory status: Not FDA-approved. Not currently a WADA-prohibited substance in the same category as recombinant GH, though GHSR agonists are under surveillance. Research organizations should verify current WADA status before use in any athletic population. Ipamorelin is not a controlled substance under the DEA Controlled Substances Act.
GH and IGF-1 elevation is theoretically capable of promoting proliferation in IGF-1R-expressing malignancies. This is a class-wide precaution consistent with all GH secretagogue compounds — not a documented adverse event specific to ipamorelin in published trials. Avoid in any research context involving active cancer or unexplained mass lesions.
Ipamorelin’s mechanism requires intact pituitary somatotroph function and normal GHSR-1a expression. Subjects with GH-secreting pituitary adenomas (acromegaly) should not receive GH secretagogue compounds. Post-radiation or surgically ablated pituitaries may have inadequate somatotroph reserve for meaningful GH response.
GH transiently reduces insulin sensitivity. In subjects with significant pre-existing glucose dysregulation, GH pulse amplification may worsen glycemic control during research protocols. Baseline fasting glucose and HbA1c monitoring is recommended. This effect is milder with ipamorelin than with GHRP-6/hexarelin since cortisol co-elevation (which further reduces insulin sensitivity) does not occur.
No safety data exists for ipamorelin in pregnancy. GH axis manipulation during pregnancy is contraindicated due to unknown effects on fetal development and placental GH dynamics. Avoid in any research context involving pregnant subjects.
Elevated insulin promotes somatostatin release, which directly suppresses pituitary GH secretion — blunting or negating Ipamorelin’s GH-stimulating effect. Any recent meal (especially carbohydrate-rich) elevates insulin and activates this brake. GLP-1 agonists (semaglutide, tirzepatide, liraglutide, etc.) compound this: they dramatically slow gastric emptying and amplify the pancreatic insulin response to meals, creating sustained insulin elevation that may persist 5-8 hours post-meal. Standard fasting windows are insufficient for GLP-1 agonist users.
Action: Administer Ipamorelin in a fasted state: minimum 2 hours post-meal, recommended 2.5-3 hours. For GLP-1 agonist users, shift to bedtime dosing where overnight fasting provides adequate clearance, or extend post-meal wait to 4-5 hours minimum for daytime dosing. Monitor glucose if concurrent hypoglycemic medications are in use.
Glucocorticoids blunt GH secretory response to GHSR-1a stimulation and promote visceral fat accumulation — working against the primary research endpoints of ipamorelin protocols.
Action: Note interaction when interpreting research outcomes. Schedule GH secretagogue protocols away from glucocorticoid administration windows where possible.
Somatostatin analogs directly antagonize pituitary GH secretion — pharmacologically negating ipamorelin’s mechanism of action by suppressing the somatotroph response to GHSR-1a activation.
Action: Contraindicated in combination — mechanistically incompatible. Do not co-administer.
Exogenous GH creates negative feedback via IGF-1 elevation, which suppresses hypothalamic GHRH secretion and increases somatostatin tone — blunting pituitary responsiveness to ipamorelin. Co-administration results in redundant mechanisms without proportional benefit.
Action: Not typically co-administered in research protocols. If exogenous GH is being studied simultaneously, note that GH secretagogue response may be attenuated.
Ipamorelin is designed as the GHRP (ghrelin receptor) component of a dual-receptor GH secretagogue protocol. Used as a monotherapy, its GH-stimulating effect is real but sub-maximal. Paired with CJC-1295 No DAC (the GHRH receptor component), the combination produces a supra-additive GH pulse that is the compounding clinic standard for pulsatile GH axis research.
Pulsatile GH optimization — body composition, sleep, recovery, and somatotropic aging research
The canonical and foundational combination — the GHRH + GHRP dual-receptor protocol. CJC-1295 No DAC activates GHRHR (Gs/cAMP pathway) while ipamorelin simultaneously activates GHSR-1a (Gq/IP3-DAG pathway). Both signals converge on pituitary somatotroph GH exocytosis, producing a GH pulse substantially greater than either compound alone. Critical timing requirement: both compounds must be injected simultaneously in the same fasted window — simultaneous injection captures the synergistic dual-receptor activation before the GHRH signal decays. This is the near-universal primary stack recommendation across all compounding clinic protocols involving ipamorelin.
Recovery and tissue repair — GH/IGF-1 systemic axis + local repair peptide coverage
Complementary recovery mechanisms. Ipamorelin drives systemic GH/IGF-1 axis amplification — anabolic, lipolytic, and repair-promoting through the endocrine cascade. BPC-157 operates via local GI-protective and tissue-healing mechanisms involving nitric oxide pathways and angiogenesis. For research protocols targeting comprehensive recovery support — connective tissue repair, GI tolerance, and systemic anabolism — the two compounds address distinct and non-redundant mechanisms simultaneously. BPC-157 may also support GI comfort during multi-peptide research protocols.
Comprehensive recovery protocols — GH/IGF-1 anabolism + systemic tissue repair and anti-inflammatory support
TB-500 (Thymosin Beta-4) provides systemic anti-inflammatory, actin sequestration, and angiogenic effects via mechanisms entirely distinct from GH/IGF-1 axis stimulation. For recovery-focused research protocols, combining systemic GH axis amplification (ipamorelin + CJC-1295 No DAC) with systemic tissue repair and anti-inflammatory support (TB-500) provides multi-mechanism coverage that addresses both the anabolic and the injury-resolution dimensions of recovery.
Oral + injectable hybrid GHSR-1a protocol — reduce injection burden while maintaining GHSR stimulation
MK-677 is an oral, long-acting GHSR-1a agonist — the same receptor arm that ipamorelin activates, but with a 24-hour half-life and oral administration. For research subjects where injection burden is a limiting factor, a hybrid protocol using ipamorelin (injected SubQ for timed pulsatile GHSR-1a activation at specific windows) combined with low-dose MK-677 (oral, sustained GHSR background) represents an alternative protocol design. However, note that co-administering two GHSR-1a agonists is mechanistically redundant — the rationale would need to be clearly defined in protocol design.
Anti-aging and metabolic optimization research — GH axis restoration + NAD+ metabolism support
For research protocols targeting comprehensive biological aging or metabolic optimization, NAD+ precursor supplementation (NMN, NR) and GH axis restoration operate through distinct but complementary mechanisms. NAD+ declines with age and supports mitochondrial function, DNA repair, and sirtuin activation. GH axis decline with age reduces anabolism, lean mass, and recovery capacity. Co-investigation of both interventions in aging-focused research addresses two distinct hallmarks of biological aging simultaneously.
All stack information is for research reference only. These combinations have not been studied in controlled trials. Individual responses vary. The CJC-1295 No DAC + Ipamorelin combination is the primary stack and the research standard; all other listed stacks are additive or complementary in rationale. Not medical advice.
Raun K, et al. (1998). Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 139(5):552–561.
PubMed: 9849822 ↗Bowers CY, et al. (1991). On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone. Endocrinology. 114(5):1537–1545.
PubMed: 2827003 ↗Howard AD, et al. (1996). A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 273(5277):974–977.
PubMed: 8637556 ↗Svensson J, et al. (1997). Two-month treatment of obese subjects with the oral growth hormone (GH) secretagogue MK-677 increases GH secretion, fat-free mass, and energy expenditure. J Clin Endocrinol Metab. 83(2):362–369.
PubMed: 9024227 ↗Veldhuis JD, et al. (2006). Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 91(12):4792–4797.
PubMed: 17018654 ↗Alba M, et al. (2006). Once-monthly administration of CJC-1295, a long-acting growth hormone-releasing hormone analog, increases growth hormone secretion in healthy adults. J Clin Endocrinol Metab. 91(3):799–805.
PubMed: 16352683 ↗Kojima M, et al. (1999). Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 402(6762):656–660.
PubMed: 10604470 ↗