Motilin: The MMC-Phase-III Hormone

TL;DR

A 22-aa hormone your gut fires every 90 minutes. The drug exploiting it is an old macrolide.
What: Motilin. 22 aa, 2,700 Da. Isolated by Brown in Vancouver, 1966. Cyclic duodenal pulses during fasting. Plasma half-life 4.5 minutes.
Does: Binds MLNR / GPR38 on enteric neurons and gastric smooth muscle. Initiates Phase III of the migrating motor complex: the sweep that clears stomach and small bowel between meals.
Evidence: Vantrappen 1979 (PMID 456224) showed exogenous motilin induces premature Phase III in fasted humans. Erythromycin hits the same receptor at sub-antimicrobial doses. Motilides (camicinal, alemcinal, atilmotin) stalled in Phase 2 from tachyphylaxis.
Used by: GI motility labs. Clinicians hit the motilin receptor with erythromycin for gastroparesis, not exogenous motilin.
Bottom line: Endogenous hormone with a textbook mechanism. The clinic prefers the accidental macrolide.

What It Is

Motilin is a 22-amino-acid linear peptide hormone with the sequence Phe-Val-Pro-Ile-Phe-Thr-Tyr-Gly-Glu-Leu-Gln-Arg-Met-Gln-Glu-Lys-Glu-Arg-Asn-Lys-Gly-Gln. Molecular weight is approximately 2,700 Da. It is synthesized and stored by enteroendocrine M-cells in the mucosa of the duodenum and proximal jejunum, with release in cyclic bursts of approximately 90–120 minutes during the fasting state. Motilin was first isolated in porcine intestine by J. C. Brown and colleagues at the University of British Columbia in 1966 during screening of intestinal extracts for motility-stimulating factors — its name derives from its motility-inducing activity.

The core biological role of motilin is as the molecular initiator of Phase III of the migrating motor complex (MMC) — the cyclical interdigestive (fasting-state) pattern of strong propagating contractions that sweep through the stomach and small intestine approximately every 90–120 minutes. The MMC has three phases: Phase I (quiescence), Phase II (irregular contractions), and Phase III (intense propagating contractions that originate in the antrum or duodenum and migrate distally). Phase III MMC activity is critical for clearing residual food, desquamated cells, and resident bacteria from the upper GI tract during fasting. Motilin plasma levels peak immediately before Phase III onset, and exogenous motilin administration reliably initiates a premature Phase III in fasted humans (Vantrappen et al., Dig Dis Sci 1979; PMID 456224).

Motilin release is exquisitely regulated: feeding suppresses motilin secretion, interrupting the MMC cycle and transitioning the GI tract to postprandial motility patterns; fasting restores motilin pulses and reestablishes MMC cycling. The release trigger is not fully elucidated but involves duodenal bile, duodenal pH, and vagal input. Motilin exerts its effects through the motilin receptor (MLNR, also known as GPR38) — a Gq-coupled seven-transmembrane receptor expressed on enteric neurons of the myenteric and submucosal plexuses and on gastric smooth muscle cells.

Motilin's clinical relevance extends to gastroparesis (where MMCs are impaired), small intestinal bacterial overgrowth / SIBO (where inadequate motility allows bacterial proliferation), functional dyspepsia, post-operative ileus, chronic intestinal pseudo-obstruction, and diabetic enteropathy. The practical therapeutic exploitation of the motilin receptor has been dominated not by exogenous motilin peptide itself but by macrolide antibiotics — erythromycin, azithromycin, and clarithromycin — which are structurally unrelated to motilin but happen to bind the motilin receptor with low-but-meaningful affinity. Erythromycin at sub-antimicrobial doses (50–250 mg) is widely used off-label as a prokinetic for gastroparesis.

Drug-development programs have pursued non-peptide motilin receptor agonists ("motilides") to capture the prokinetic effect without macrolide antimicrobial properties or tachyphylaxis. Camicinal (GSK962040), alemcinal (ABT-229), and atilmotin (KC-11458) all reached Phase II. None has reached approval as of 2026 — the most consistent limitation has been rapid tachyphylaxis at the motilin receptor with chronic exposure, undercutting long-term efficacy.

Mechanism of Action

Motilin's mechanism centers on motilin receptor (MLNR / GPR38) activation on enteric neurons and gastric smooth muscle. The downstream effect is phase-specific GI contractile activity.

MLNR / GPR38 activation — Motilin binds MLNR with high affinity on cholinergic enteric neurons of the myenteric plexus and on gastric smooth muscle cells. Gq coupling drives phospholipase C → IP3/DAG → intracellular calcium mobilization → smooth muscle contraction.
Phase III MMC initiation — The signature motilin effect. Endogenous motilin pulses immediately precede Phase III MMC onset; exogenous motilin induces premature Phase III in fasted human subjects (Vantrappen 1979; Peeters 1992). This is the primary biological role and the foundation of the clinical relevance.
Gastric emptying acceleration — Motilin promotes antral and pyloric contractions, accelerating gastric emptying of both solids and liquids. This underlies its relevance to gastroparesis and the rationale for motilin-receptor-agonist drug development.
Lower esophageal sphincter effects — Motilin increases lower esophageal sphincter pressure in some models; contribution to human LES tone is considered minor compared to other regulators.
Duodenal mucosal M-cell secretion — Motilin is synthesized and stored in M-cells of duodenal and proximal jejunal crypts. Release is suppressed by meals and restored during fasting — the neural and humoral signals triggering release involve vagal activity, bile reaching the duodenum, and duodenal pH sensing.
Short plasma half-life — Endogenous motilin has a plasma half-life of approximately 4.5 minutes, consistent with its role as a pulsatile acute regulator rather than a sustained-action hormone. Exogenous motilin pharmacokinetics match this short exposure window.
Erythromycin as exogenous agonist — Erythromycin and other macrolide antibiotics bind MLNR with lower affinity than native motilin but with enough potency to produce clinically useful prokinetic effect at sub-antimicrobial doses (50–250 mg). This is the basis of off-label macrolide prokinetic use in gastroparesis.
Tachyphylaxis at the motilin receptor — Chronic motilin or motilin-agonist exposure rapidly desensitizes the motilin receptor, producing tachyphylaxis within days of continuous dosing. This receptor-level adaptation is the dominant limitation in all motilin and motilide development programs.
Interaction with ghrelin signaling — Motilin and ghrelin are structurally related peptides (motilin is the evolutionary precursor of ghrelin; they share ancestral gene architecture). Motilin and ghrelin receptors are closely related paralogs. There is meaningful cross-regulation between the two pathways in the proximal GI tract.
Central appetite modulation (modest) — Motilin has been implicated in fasting-state hunger sensation, though the contribution is smaller than ghrelin's. The "hungry stomach growling" sensation of the MMC Phase III ("borborygmus") is motilin-driven.

What the Research Shows

Motilin has an unusually deep physiology literature stretching back to the 1970s, concentrated in GI motility research. Exogenous motilin therapeutic development has been limited by tachyphylaxis.

Foundational discovery (Brown et al., 1966) — Isolation and characterization of motilin from porcine duodenal extracts at the University of British Columbia.
MMC Phase III initiation (Vantrappen et al., Dig Dis Sci 1979; PMID 456224) — "Motilin and the interdigestive migrating motor complex in man." Demonstrated that plasma motilin peaks immediately before Phase III MMC onset and that exogenous motilin initiates Phase III in fasted subjects. Foundational paper for the MMC-motilin association.
Peeters 1992 pattern characterization — Comprehensive physiological characterization of the fasting motilin/MMC pattern in humans.
Gastroparesis and erythromycin (Tack et al., Gastroenterology 2005; PMID 15825084) — Comprehensive review of motilin and erythromycin in gastroparesis. Establishes erythromycin 50–250 mg 2–3× daily as the standard off-label prokinetic use.
Camicinal Phase II (GSK962040, various reports) — Oral non-peptide motilin receptor agonist. Demonstrated acceleration of gastric emptying in diabetic gastroparesis and critical-care feeding-intolerance populations in Phase II. Development discontinued before Phase III.
Alemcinal (ABT-229) Phase II — Macrolide-derived motilin agonist from Abbott. Demonstrated efficacy in diabetic gastroparesis but showed unacceptable tachyphylaxis; development halted.
Atilmotin (KC-11458) Phase II — Kodama motilin agonist; Phase II trials demonstrated short-term gastric emptying acceleration in diabetic gastroparesis; did not advance.
Mitemcinal (GM-611) — Oral erythromycin-derived motilin agonist from Chugai; Phase II/III development in diabetic gastroparesis; primary endpoints narrowly missed, development halted.
Motilin receptor cloning (Feighner et al., Science 1999; PMID 10400997) — Identification and cloning of the motilin receptor (MLNR/GPR38) as a distinct G-protein-coupled receptor. Foundational for subsequent drug development.
Motilin-receptor knockout studies — Animal models with motilin receptor deletion demonstrate absent or severely impaired MMC Phase III activity, confirming motilin's non-redundant role.
SIBO correlation — Clinical studies correlate impaired MMC function (secondary to diabetes, gastroparesis, scleroderma, or chronic opioid use) with small intestinal bacterial overgrowth. Motilin-receptor-agonist therapy as a SIBO treatment remains investigational.
Functional dyspepsia overlap — Subsets of functional dyspepsia patients show motilin pattern abnormalities; translational relevance to symptom management unclear.

Research Limitations

Motilin's physiology is well-established from decades of GI research. Clinical application has been limited by two factors: (1) rapid tachyphylaxis at the motilin receptor, which has defeated multiple drug-development programs; and (2) the practical availability of erythromycin and azithromycin as motilin agonists, which satisfies most clinical prokinetic needs without the development cost of a novel motilide. There is no active pharmaceutical sponsor advancing exogenous motilin peptide toward approval, and motilin remains a research-tool peptide rather than a therapeutic.

Human Data

Motilin human data is dominated by physiology studies and clinical trials of motilin receptor agonists rather than exogenous motilin peptide.

Vantrappen 1979 MMC physiology (PMID 456224) — Core physiological characterization of motilin and MMC in humans.
Peeters 1992 pattern studies — Comprehensive fasting-state motilin pulse characterization.
Erythromycin prokinetic trials (multiple) — Decades of controlled and open-label clinical trial data establishing erythromycin 50–250 mg as an off-label gastroparesis prokinetic via motilin receptor agonism.
Azithromycin prokinetic trials — Similar mechanism; longer QT-safety margin than erythromycin; common macrolide prokinetic choice in modern GI practice.
Camicinal Phase II (gastroparesis + enteral feeding intolerance) — Multiple GSK-sponsored Phase II trials demonstrating motilin receptor agonist efficacy; not advanced.
ABT-229 alemcinal Phase II (diabetic gastroparesis) — Tachyphylaxis dominated the program.
Mitemcinal (GM-611) Phase III (diabetic gastroparesis) — Primary endpoint narrowly missed; development halted.
SIBO motility hypothesis studies — Observational correlation between impaired MMC activity and SIBO; motilin-axis therapy remains investigational.
Critical care ICU feeding-intolerance studies — Motilin agonists studied as adjuncts to enteral feeding tolerance in ICU populations; mixed results and short-duration benefit due to tachyphylaxis.
No community / optimization human use — Motilin is not a peptide sold in research-peptide channels for cosmetic or optimization goals. The profile exists for physiology and pharmacology context.

Dosing from the Literature

Dosing information below reflects research-context administration of motilin peptide and clinical dosing of motilin receptor agonists. Motilin peptide itself is not a community-use product.

Context	Dose	Route / Frequency	Notes
Research (MMC induction studies)	~0.2–1.0 μg/kg/min infusion	IV continuous infusion	Vantrappen 1979 and subsequent physiology studies. Fasted subject; induces premature Phase III.
Erythromycin (off-label prokinetic)	50–250 mg	Oral, 2–3× daily before meals	Sub-antimicrobial motilin-receptor agonism dose; standard gastroparesis off-label use.
Erythromycin (IV acute)	3 mg/kg	IV single dose over 20 min	Critical-care enteral feeding intolerance; 3 mg/kg IV accelerates gastric emptying.
Azithromycin (off-label prokinetic)	250 mg	Oral once daily	Alternative macrolide prokinetic; longer QT-safety margin.
Camicinal (Phase II, investigational)	25–150 mg	Oral daily	GSK962040; not approved.
Mitemcinal (Phase III, investigational)	10 mg	Oral BID	GM-611; not approved.

Dosing Disclaimer

Exogenous motilin peptide is not a clinical therapy. The only clinically used motilin-axis agents are the macrolide antibiotics erythromycin and azithromycin at sub-antimicrobial prokinetic doses, used off-label for gastroparesis. Tachyphylaxis limits the useful duration of any motilin receptor agonist to weeks rather than months of continuous therapy. Erythromycin and azithromycin carry QT-prolongation risk — concurrent use with other QT-prolonging drugs, or in patients with long-QT syndrome, is contraindicated.

Reconstitution & Storage

Motilin peptide is available from research-peptide vendors as lyophilized powder for laboratory use only. There is no community-dosing pattern because motilin is not used for human optimization.

Format	Supply	Preparation	Use Context
Lyophilized research peptide	1 mg vial (typical)	1 mL sterile water or BAC water → 1 mg/mL	Research use; GI motility physiology studies.
Erythromycin IV	500 mg powder vial	Diluted per hospital pharmacy protocol; typical 3 mg/kg infusion	Hospital prokinetic use; gastroparesis acute.
Erythromycin oral suspension	200 mg/5 mL or 400 mg/5 mL	Ready-to-use	Chronic off-label prokinetic dosing.
Azithromycin oral tablet	250 mg tablets	Ready-to-use	Alternative chronic off-label prokinetic dosing.

Motilin peptide storage — 2–8°C unreconstituted; −20°C for long-term. Reconstituted solution: 2–8°C, use within days. Fragile; oxidation-sensitive.
Research administration — Continuous IV infusion via pump; single-bolus administration does not recapitulate endogenous pulse biology.
Erythromycin / azithromycin storage — Room temperature; oral suspensions refrigerated post-reconstitution per manufacturer.
QT monitoring when using macrolide prokinetics — Baseline ECG in patients with any cardiac history; avoid concurrent QT-prolonging agents.
Practical clinical use — Community / optimization users do not have legitimate access to motilin peptide. Erythromycin and azithromycin prokinetic use is a clinical prescription decision, not a self-protocol.

→ Use the Kalios Dosing Calculator for research conversions

Side Effects & Risks

Important

Research-only peptide. Exogenous motilin produces rapid tachyphylaxis and is not a consumer product. Share this with your clinician before exploring prokinetic options.

Side-effect information synthesizes exogenous motilin peptide research data and the well-characterized erythromycin / azithromycin prokinetic profile.

GI cramping — Expected on-target effect of enhanced motility. Dose-dependent and typically self-limited.
Nausea (paradoxical) — Excessive motilin agonism can produce nausea despite the prokinetic mechanism — MMC Phase III initiated outside physiological context can be subjectively unpleasant.
Tachyphylaxis — The dominant therapeutic limitation. Motilin receptor desensitizes rapidly with chronic exposure, blunting efficacy within days to weeks.
Abdominal pain — Reported in a subset of users of macrolide prokinetics; usually dose-related.
Diarrhea — Both from the prokinetic effect and (for macrolides) from antibiotic-mediated gut flora disruption.
QT prolongation (macrolide prokinetics) — Erythromycin and to a lesser extent azithromycin prolong the QT interval. Clinically significant in patients with long-QT syndrome, concurrent QT-prolonging medications (fluoroquinolones, tricyclics, ondansetron, methadone, certain antipsychotics), hypokalemia, or hypomagnesemia. Torsade de pointes has been reported.
Antimicrobial resistance (macrolides) — Chronic sub-antimicrobial erythromycin and azithromycin use at prokinetic doses contributes to macrolide resistance selection pressure; a well-documented population-level concern.
Drug interactions (macrolides) — Erythromycin is a potent CYP3A4 inhibitor; interacts with statins, warfarin, certain calcium channel blockers, and many other drugs. Azithromycin has a cleaner interaction profile.
Hepatotoxicity (macrolides) — Rare but documented; monitor LFTs in chronic use.
Hearing loss (rare, high-dose IV erythromycin) — Reversible ototoxicity at high IV macrolide doses.
Pregnancy and lactation — Macrolides are pregnancy Category B. Exogenous motilin peptide has not been studied in pregnancy.
C. difficile risk (macrolides) — Any antibiotic exposure carries C. difficile colitis risk; less pronounced with macrolides than with clindamycin or fluoroquinolones but present.

Motilin Receptor Agonist Drug Development — A Brief History

The motilin receptor has been a pharmaceutical target for gastroparesis and related dysmotility disorders for over three decades, with repeated development attempts running aground on tachyphylaxis.

Erythromycin rediscovery (1980s) — Macrolide antibiotics were observed to cause GI cramping as an antimicrobial side effect in the 1950s–1970s. In the 1980s this was traced to motilin receptor agonism. Janssens 1990 NEJM formalized erythromycin's prokinetic use in gastroparesis.
Motilide program 1 — Abbott ABT-229 (alemcinal) — Late 1990s; advanced through Phase II for diabetic gastroparesis. Demonstrated gastric emptying acceleration but efficacy waned rapidly with chronic dosing. Program terminated due to tachyphylaxis.
Motilide program 2 — Chugai GM-611 (mitemcinal) — Late 1990s–2000s; erythromycin-derived oral motilide. Reached Phase III for diabetic gastroparesis. Primary endpoint narrowly missed; development halted.
Motilide program 3 — Kodama KC-11458 (atilmotin) — Phase II in diabetic gastroparesis; short-term acceleration of gastric emptying. Not advanced.
Motilide program 4 — GSK GSK962040 (camicinal) — 2010s; non-peptide, selective motilin receptor agonist. Phase II in diabetic gastroparesis and in critical-care enteral-feeding intolerance. Effective short-term; discontinued.
Shared failure mode — tachyphylaxis — Every program has encountered rapid motilin receptor desensitization within days of chronic dosing. This is receptor biology, not a drug-specific limitation. It may require pulsatile dosing rather than continuous infusion / oral to fully solve.
Ghrelin receptor agonist programs (overlap) — The motilin and ghrelin receptors are paralogs; ghrelin receptor agonists (relamorelin from Allergan, TZP-102, ulimorelin) have been pursued for similar indications with similar tachyphylaxis challenges.
Current standard of care — Erythromycin and azithromycin at sub-antimicrobial prokinetic doses remain the clinical motilin-axis therapies. Metoclopramide (D2 antagonist) and prucalopride (5-HT4 agonist) serve as complementary or sequential prokinetics where appropriate.

Bloodwork & Monitoring

Comprehensive metabolic panel — Baseline liver and renal function. Macrolide prokinetics can elevate hepatic enzymes; renal clearance is relevant for erythromycin dosing.
CBC — Standard baseline screening.
Baseline ECG — For any patient initiating macrolide prokinetic therapy, particularly in those with cardiac history or on concurrent QT-prolonging medications. Evaluate QTc.
Electrolytes (K, Mg) — Hypokalemia and hypomagnesemia amplify QT-prolongation risk; correct before macrolide initiation.
Gastric emptying study — Scintigraphic gastric emptying is the standard baseline for evaluating treatment response in gastroparesis.
Symptom diary / GCSI (Gastroparesis Cardinal Symptom Index) — Validated patient-reported outcome for gastroparesis; baseline and follow-up for clinical response tracking.
SIBO breath testing — Lactulose or glucose hydrogen/methane breath test if SIBO is suspected as a motility consequence.
Diabetes management (diabetic gastroparesis) — HbA1c and glycemic control are the most important modifiable factors for diabetic gastroparesis; pharmacologic prokinetics are adjunctive.
Chronic macrolide use — Periodic LFTs, electrolytes, ECG if QTc was borderline at baseline.

Commonly Stacked With

Motilin axis therapy (practically, macrolide prokinetics) is typically used in clinical gastroparesis management alongside lifestyle and dietary interventions; "stacking" applies to the clinical armamentarium rather than a community protocol.

Metoclopramide (dopamine D2 antagonist)

FDA-approved prokinetic for gastroparesis via D2 receptor antagonism and 5-HT4 agonism. Often sequenced with or alternated with macrolide prokinetics to address tachyphylaxis. Carries tardive dyskinesia risk with chronic use — black-box-warning-limited to 12 weeks.

Prucalopride (5-HT4 agonist)

Selective 5-HT4 agonist approved for chronic idiopathic constipation; off-label use in gastroparesis. Mechanism complementary to motilin-receptor agonism. Safer than older 5-HT4 agonists (tegaserod, cisapride).

Dietary modifications (small frequent meals, low fat, low fiber)

Non-pharmacologic foundation of gastroparesis management. Amplifies the utility of any prokinetic; without dietary adjustment, pharmacologic response tends to be modest.

Antiemetics (ondansetron, prochlorperazine)

Symptom management for gastroparesis-associated nausea. Use caution with ondansetron + macrolide combination — additive QT-prolongation risk.

Rifaximin (SIBO-directed)

Non-absorbed antibiotic for small intestinal bacterial overgrowth secondary to impaired motility. Addresses the downstream consequence of MMC failure rather than the motility deficit itself.

→ Check compound compatibility in the Stack Builder

Regulatory Status

Current Status — April 2026

Motilin peptide is not FDA-approved as a therapeutic agent. It is available as a research peptide for laboratory investigation only. No pharmaceutical sponsor is currently advancing exogenous motilin peptide toward approval.

The motilin receptor (MLNR / GPR38) is clinically targeted with erythromycin and azithromycin — FDA-approved macrolide antibiotics used off-label at sub-antimicrobial prokinetic doses for gastroparesis. These are the practical clinical motilin-axis therapies.

Non-peptide motilin receptor agonists (camicinal / GSK962040, alemcinal / ABT-229, atilmotin / KC-11458, mitemcinal / GM-611) have advanced through Phase II and some through Phase III without reaching approval. Development has been repeatedly limited by tachyphylaxis.

Motilin is not on the WADA Prohibited List. It is not on the FDA Category 2 Bulk Drug Substances list and is not part of HHS Secretary Kennedy's February 2026 Category 2 peptide reclassification announcement.

Exogenous motilin is not a community-use compound. The profile exists for physiology and pharmacology context for users investigating GI motility literature or motilin receptor agonist drug development.

Cost & Access

Motilin peptide is available through scientific supply houses (Bachem, Tocris, Sigma-Aldrich, Phoenix Pharmaceuticals) for laboratory research use only. It is not dispensed for human therapeutic use.

Erythromycin and azithromycin (the clinical motilin-axis therapies) are widely available generic prescription antibiotics. At sub-antimicrobial prokinetic doses, they are prescribed off-label by gastroenterologists and internists for gastroparesis and refractory functional dyspepsia. Coverage is typically straightforward given the generic status.

Motilin is not among the peptides addressed by HHS Secretary Kennedy's February 2026 Category 2 reclassification announcement. It has never been Category 2 because it has never been a serious compounding candidate — clinical demand is already served by macrolide antibiotics. Regulatory status is unlikely to change absent a sponsor reviving motilin-peptide or motilide development.

Estimated pricing and access as of April 2026. Actual costs vary by provider, location, and prescription status. Kalios does not sell compounds.

Related Compounds

People researching Motilin often also look at these:

Nesfatin-1

Hypothalamic 82-amino-acid satiety peptide derived from NUCB2.

GHRP-2

Second-generation growth hormone releasing peptide. Stronger GH pulse than ipamorelin with mild prolactin rise.

GHRP-6

Ghrelin-receptor agonist with strong appetite-stimulating effect alongside GH release.

BPC-157

15-amino-acid pentadecapeptide. The most-studied tissue-repair peptide with broad tendon, ligament, gut, and neural healing effects.

Insulin

Peptide hormone regulating glucose uptake and anabolism. The foundational metabolic peptide.

Next Steps

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Key References

Vantrappen G, Janssens J, Peeters TL, Bloom SR, Christofides ND, Hellemans J. Motilin and the interdigestive migrating motor complex in man. Dig Dis Sci. 1979;24(7):497-500. PMID: 456224. DOI: 10.1007/BF01489315.
Brown JC, Mutt V, Dryburgh JR. The further purification of motilin, a gastric motor activity stimulating polypeptide from the mucosa of the small intestine of hogs. Can J Physiol Pharmacol. 1971;49(5):399-405. PMID: 5119416.
Tack J, Janssens J, Vantrappen G, Peeters T, Annese V, Depoortere I, Muls E, Bouillon R. Effect of erythromycin on gastric motility in controls and in diabetic gastroparesis. Gastroenterology. 2005;128(4):1040-1053. PMID: 15825084.
Peeters TL, Vantrappen G, Janssens J. Fasting plasma motilin levels are related to the interdigestive motility complex. Gastroenterology. 1980;79(4):716-719. PMID: 7409390.
Feighner SD, Tan CP, McKee KK, Palyha OC, Hreniuk DL, Pong SS, Austin CP, Figueroa D, MacNeil D, Cascieri MA, Nargund R, Bakshi R, Abramovitz M, Stocco R, Kargman S, O'Neill G, Van Der Ploeg LH, Evans J, Patchett AA, Smith RG, Howard AD. Receptor for motilin identified in the human gastrointestinal system. Science. 1999;284(5423):2184-2188. PMID: 10400997. DOI: 10.1126/science.284.5423.2184.
Sanger GJ, Wang Y, Hobson A, Broad J. Motilin: towards a new understanding of the gastrointestinal neuropharmacology and therapeutic use of motilin receptor agonists. Br J Pharmacol. 2013;170(7):1323-1332. PMID: 23189978.
Janssens J, Peeters TL, Vantrappen G, Tack J, Urbain JL, De Roo M, Muls E, Bouillon R. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. Preliminary studies. N Engl J Med. 1990;322(15):1028-1031. PMID: 2320066.
Sudo H, Yamada K, Ito K, Omura S, Itoh Z. Effects of mitemcinal (GM-611), a new orally active erythromycin-derived prokinetic agent, on delayed gastric emptying. J Pharmacol Exp Ther. 2007;322(1):1-8. PMID: 17392402.
Broad J, Sanger GJ. The antibiotic azithromycin is a motilin receptor agonist in human stomach: comparison with erythromycin. Br J Pharmacol. 2013;168(8):1859-1867. PMID: 23190027.
Dhir R, Richter JE. Erythromycin in the short- and long-term control of dyspepsia symptoms in patients with gastroparesis. J Clin Gastroenterol. 2004;38(3):237-242. PMID: 15128071.
Chapman MJ, Fraser RJ, Matthews G, Russo A, Bellon M, Besanko LK, Jones KL, Butler R, Chatterton B, Horowitz M. Glucose absorption and gastric emptying in critical illness. Crit Care. 2009;13(4):R140. PMID: 19712472.
Hellström PM, Tack J, Johnson LV, Hacquoil K, Barton ME, Richards DB, Alpers DH, Sanger GJ, Dukes GE. The pharmacodynamics, safety and pharmacokinetics of single doses of the motilin agonist, camicinal, in type 1 diabetes mellitus with slow gastric emptying. Br J Pharmacol. 2016;173(11):1768-1777. PMID: 26924601.
Camilleri M, Parkman HP, Shafi MA, Abell TL, Gerson L; American College of Gastroenterology. Clinical guideline: management of gastroparesis. Am J Gastroenterol. 2013;108(1):18-37. PMID: 23147521.
Poitras P, Peeters TL. Motilin. Curr Opin Endocrinol Diabetes Obes. 2008;15(1):54-57. PMID: 18185064.
Sanger GJ, Westaway SM, Barnes AA, Macpherson DT, Muir AI, Jarvie EM, Bolton VN, Cellek S, Näslund E, Hellström PM, Borman RA, Unmack MA, Hansen MB, Knowles CH, Lindberg G, Goldstone AP, Winchester WJ. GSK962040: a small molecule, selective motilin receptor agonist, effective as a stimulant of human and rabbit gastrointestinal motility. Neurogastroenterol Motil. 2009;21(6):657-664. PMID: 19220757.
Hocart SJ, Reddy V, Murphy WA, Coy DH. Three-dimensional quantitative structure-activity relationships of somatostatin and motilin receptors. J Med Chem. 1995;38(11):1974-1989. PMID: 7783127.

Last updated: April 2026 | Profile authored by Kalios Peptides research team

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