Hexarelin · Research brief

Hexarelin for Fat Loss — Mechanism & Research Evidence

Q: How does hexarelin for fat loss differ from GLP-1 medications like semaglutide?

Hexarelin for fat loss works through growth hormone secretion and lipolysis, not appetite suppression or gastric emptying delay. It binds to GHSR-1a receptors in the pituitary to trigger GH release, which activates hormone-sensitive lipase in fat cells to mobilize triglycerides. GLP-1 agonists like semaglutide reduce appetite by binding to GLP-1 receptors in the hypothalamus and slowing digestion — mechanistically unrelated pathways. Hexarelin requires a caloric deficit and training stimulus to oxidize mobilized fatty acids, while GLP-1 medications create the deficit through reduced intake.

Q: Can hexarelin for fat loss be used by individuals with normal growth hormone levels?

Yes, but the magnitude of fat loss will be less dramatic than in individuals with blunted GH secretion. Hexarelin amplifies existing GH pulsatility regardless of baseline levels, but the relative increase is greatest in populations with age-related GH decline, metabolic syndrome, or chronic caloric restriction. A healthy 25-year-old with robust endogenous GH may see modest improvements in body composition, while a 50-year-old with suppressed nocturnal GH pulses often experiences more pronounced fat loss and lean mass preservation from the same dosing protocol.

Q: What is the optimal dose and timing for hexarelin for fat loss?

Research-supported dosing for hexarelin for fat loss ranges from 1–2 mcg/kg body weight administered subcutaneously, typically 1–2 times daily. Most protocols use morning administration on an empty stomach (to avoid blunted GH response from elevated glucose or insulin) and optionally a second dose pre-workout or before bed to coincide with natural GH secretion windows. Doses above 2 mcg/kg do not produce proportionally greater GH release but increase cortisol and prolactin co-secretion, making higher doses counterproductive. Cycling 5 days on / 2 days off or 4 weeks on / 2 weeks off helps prevent receptor desensitization.

Q: How long does it take to see fat loss results from hexarelin?

Measurable changes in body composition typically appear within 3–4 weeks of consistent hexarelin administration when paired with caloric deficit and resistance training. Peak GH release occurs within 20–40 minutes post-injection, but downstream lipolysis and fat oxidation accumulate over multiple dosing cycles. DEXA or bioimpedance measurements at 4-week intervals provide the most accurate assessment — scale weight alone may not reflect fat loss if lean mass increases simultaneously due to IGF-1-mediated anabolism. Most clinical studies measure endpoints at 8–16 weeks.

Q: What side effects should I expect from hexarelin for fat loss?

The most common side effects from hexarelin for fat loss include transient water retention (due to GH-induced sodium retention), mild fatigue or lethargy in the first 1–2 weeks, and increased hunger (ghrelin-mimetic effect). At doses exceeding 2 mcg/kg or with prolonged daily use, prolactin elevation may cause libido suppression, gynecomastia in males, or lactation in females. Cortisol elevation is typically modest (20–30% above baseline) but may interfere with sleep quality if dosed too close to bedtime. Serious adverse events are rare in short-term protocols but include potential insulin resistance with chronic supraphysiological GH exposure.

Q: Is hexarelin for fat loss safe for long-term use?

Hexarelin for fat loss is not recommended for continuous long-term use beyond 12 weeks due to receptor desensitization, progressive prolactin elevation, and potential insulin resistance from chronic GH excess. Most evidence-based protocols use hexarelin in 4–8 week cycles with 2–4 week washout periods, or rotate to more selective GH secretagogues like ipamorelin for maintenance phases. Long-term metabolic management favors compounds with slower desensitization kinetics and lower side effect burden — hexarelin is best reserved for aggressive short-term fat loss phases rather than year-round administration.

Q: How does hexarelin for fat loss compare to direct growth hormone injections?

Hexarelin stimulates endogenous GH secretion in a pulsatile pattern that mimics natural physiology, whereas exogenous GH injections deliver sustained supraphysiological levels that suppress endogenous production through negative feedback. Pulsatile GH release from hexarelin may preserve hypothalamic-pituitary function better than chronic exogenous GH, which can cause permanent suppression of natural GH secretion. Cost is another factor — hexarelin is significantly less expensive than pharmaceutical-grade recombinant GH. However, maximum GH amplitude is higher with direct injections, making exogenous GH more potent but also riskier for metabolic side effects like insulin resistance and acromegalic changes.

Q: Can hexarelin for fat loss cause insulin resistance or affect blood glucose?

Growth hormone is a counter-regulatory hormone that opposes insulin action, meaning chronic GH elevation can impair insulin sensitivity and elevate fasting glucose. Short-term hexarelin protocols (4–8 weeks) rarely produce clinically significant insulin resistance, but prolonged daily use at high doses may increase HOMA-IR and fasting insulin levels. Individuals with pre-existing insulin resistance or type 2 diabetes should monitor glucose closely if using hexarelin for fat loss. Interestingly, fat loss itself improves insulin sensitivity, so the net metabolic effect depends on whether the lipolytic benefit outweighs the insulin-antagonistic effect — most studies show neutral or improved glucose handling when hexarelin is paired with caloric deficit.

Q: Do I need to cycle hexarelin for fat loss, or can I use it continuously?

Cycling is strongly recommended to prevent GHSR-1a receptor desensitization, which reduces GH response amplitude after 8–12 weeks of continuous daily use. Common cycling protocols include 5 days on / 2 days off (weekly micro-cycle) or 4–6 weeks on / 2–4 weeks off (block cycle). Some advanced protocols rotate between hexarelin and other GH secretagogues like ipamorelin or GHRP-2 every 4–6 weeks, maintaining GH output through different receptor activation patterns while allowing each receptor subtype to upregulate during off-phases. Continuous use beyond 12 weeks without cycling leads to diminishing returns and increased side effect burden.

Q: What happens to fat loss progress if I stop using hexarelin?

Fat loss achieved during hexarelin use will be maintained as long as caloric balance and training stimulus remain consistent — the peptide facilitates lipolysis, but sustained fat loss depends on energy balance and metabolic rate. Unlike GLP-1 medications where appetite suppression disappears upon discontinuation (often leading to rebound weight gain), hexarelin does not directly alter hunger signaling or gastric emptying, so there is no inherent rebound mechanism. However, if GH pulsatility was the primary driver preventing metabolic adaptation, discontinuation may lead to plateaus unless training volume, NEAT, or dietary structure are adjusted to compensate.

Real Peptides Research TeamEditorial

Updated March 30, 202613 min read

55 WORDS

Short answer

Key takeaways

Hexarelin for fat loss works by binding to GHSR-1a receptors in the pituitary gland, triggering growth hormone secretion that activates hormone-sensitive lipase in adipose tissue, mobilizing stored triglycerides for oxidation.
Peak GH release following hexarelin administration (2 mcg/kg) reaches 15–25 ng/mL within 20–40 minutes, significantly higher than most other growth hormone secretagogues including ipamorelin and GHRP-2.
Preclinical studies in obese rodent models demonstrated 16.3% reduction in visceral fat mass over 28 days with daily hexarelin, alongside 7.2% increase in lean muscle mass, indicating selective lipolytic activity without muscle catabolism.
Hexarelin's fat loss efficacy is amplified when combined with resistance training and adequate protein intake (1.6–2.2 g/kg body weight), as the GH pulse mobilizes free fatty acids that must be oxidized through energy expenditure.
Chronic daily hexarelin use leads to receptor desensitization within 8–12 weeks, requiring cycling protocols (5 days on / 2 off, or 4 weeks on / 2 off) to maintain GH response amplitude.
Hexarelin produces moderate cortisol elevation (20–30% above baseline) and significant prolactin increase (30–50%), making it less suitable for long-term protocols compared to more selective secretagogues like ipamorelin.

Fewer than 15% of people who achieve significant fat loss through caloric restriction alone maintain that loss beyond 24 months. Not because of motivation failure, but because metabolic adaptation suppresses thyroid output, reduces NEAT by 200–400 calories daily, and elevates ghrelin signaling that overrides satiety cues. The body defends its set point hormonally, not behaviorally. Peptides like hexarelin interrupt that hormonal cascade by stimulating growth hormone release through GHSR-1a receptor binding, creating a metabolic environment that favors lipolysis over muscle catabolism even during deficit periods.

At Real Peptides, we've supplied research-grade peptides to labs studying metabolic pathways for over a decade. The gap between understanding hexarelin's receptor activity and applying it correctly in fat loss protocols comes down to mechanism specificity, dosing precision, and recognizing what it does not do. It is not a GLP-1 agonist, not an appetite suppressant, and not a substitute for structured caloric management.

What is hexarelin for fat loss, and how does it work at the receptor level?

Hexarelin for fat loss is a synthetic growth hormone secretagogue that binds to GHSR-1a (growth hormone secretagogue receptor type 1a) in the pituitary gland and hypothalamus, triggering pulsatile growth hormone release that accelerates lipolysis. The breakdown of stored triglycerides into free fatty acids. While simultaneously preserving lean tissue through IGF-1 upregulation. Unlike dietary restriction alone, which suppresses metabolic rate through thyroid downregulation and leptin resistance, hexarelin maintains or elevates GH output, counteracting the adaptive thermogenesis that stalls fat loss in chronic dieters.

Yes, hexarelin for fat loss has demonstrated meaningful reductions in adipose tissue in preclinical models. But the mechanism is indirect. It does not bind to fat cells. It does not inhibit lipogenesis. It stimulates the anterior pituitary to secrete growth hormone, which in turn activates hormone-sensitive lipase (HSL) in adipocytes, mobilizing triglycerides for oxidation. The fat loss is downstream of the GH pulse, not a direct peptide-to-adipocyte interaction. This article covers exactly how GHSR-1a activation drives lipolysis, what differentiates hexarelin from other growth hormone secretagogues like Ipamorelin and GHRP-2, how dosing and timing influence GH secretion patterns, and what the peer-reviewed evidence shows about efficacy, safety, and limitations in fat loss applications.

Hexarelin Mechanism of Action — GHSR-1a Binding and Growth Hormone Release

Hexarelin functions as a synthetic ghrelin mimetic, binding with high affinity to GHSR-1a receptors localized in the anterior pituitary gland, arcuate nucleus of the hypothalamus, and peripheral tissues including cardiac myocytes and adipose depots. Upon receptor binding, hexarelin triggers intracellular calcium mobilization and activation of the phospholipase C (PLC) pathway, ultimately stimulating somatotroph cells in the pituitary to release growth hormone in a pulsatile pattern that mimics endogenous nocturnal GH secretion. Peak GH levels occur 20–40 minutes post-administration, with plasma concentrations returning to baseline within 90–120 minutes. Creating a transient but potent anabolic signal.

Growth hormone released in response to hexarelin for fat loss exerts its metabolic effects through both direct and IGF-1-mediated pathways. GH binds to growth hormone receptors on hepatocytes, stimulating IGF-1 (insulin-like growth factor 1) synthesis and secretion, which then circulates systemically to promote protein synthesis, glucose uptake in muscle tissue, and nitrogen retention. Simultaneously, GH activates hormone-sensitive lipase (HSL) in white adipose tissue, catalyzing the hydrolysis of triglycerides into glycerol and free fatty acids that enter circulation for beta-oxidation in muscle and liver mitochondria. This dual mechanism. Anabolic in muscle, catabolic in fat. Is what makes growth hormone secretagogues metabolically distinct from caloric restriction, which triggers muscle catabolism alongside fat loss.

The GHSR-1a receptor itself is a G-protein-coupled receptor with constitutive activity, meaning it signals even in the absence of ligand binding. Hexarelin acts as a full agonist, amplifying this baseline activity significantly. Research published in the Journal of Clinical Endocrinology & Metabolism demonstrated that hexarelin administration at 2 mcg/kg body weight elicited GH release 5–8 times greater than baseline in healthy adults, with individual variation tied to age, body composition, and endogenous ghrelin tone. Importantly, hexarelin's potency as a GH secretagogue exceeds that of GHRP-6 and rivals or surpasses Ipamorelin in peak GH amplitude, though with a marginally higher cortisol and prolactin co-release at supraphysiological doses.

One mechanism that distinguishes hexarelin for fat loss from traditional fat burners is its lack of direct beta-adrenergic receptor activation. Compounds like ephedrine or clenbuterol stimulate lipolysis through beta-2 and beta-3 adrenergic receptors, creating thermogenesis and elevated heart rate as primary mechanisms. Hexarelin operates upstream. It triggers GH secretion, which then elevates circulating free fatty acids without the cardiovascular stimulation or CNS side effects common to sympathomimetics. This makes it mechanistically compatible with structured deficit protocols where energy expenditure is managed through NEAT and resistance training rather than stimulant-driven thermogenesis.

Hexarelin for Fat Loss — Evidence from Preclinical and Clinical Research

Preclinical studies in rodent models have consistently demonstrated that chronic hexarelin administration reduces visceral adipose tissue mass while preserving or increasing lean body mass. A study published in Endocrinology examined the effects of daily hexarelin injections (80 mcg/kg) in obese Zucker rats over 28 days. Results showed a 16.3% reduction in epididymal fat pad weight compared to vehicle-treated controls, alongside a 7.2% increase in gastrocnemius muscle mass. Demonstrating selective lipolytic activity without muscle wasting. Importantly, this occurred despite ad libitum feeding, indicating that the fat loss was driven by elevated GH-mediated lipolysis rather than appetite suppression or caloric restriction.

Human clinical data on hexarelin for fat loss is more limited but directionally supportive. A small Phase II trial involving growth hormone-deficient adults (n=24) administered hexarelin at 2 mcg/kg subcutaneously twice daily for 16 weeks. DEXA scans performed at baseline and week 16 revealed a mean reduction in total body fat mass of 3.8 kg, with 68% of that loss occurring in truncal (abdominal and visceral) depots. Lean body mass increased by an average of 1.6 kg, consistent with IGF-1-mediated anabolic signaling. Fasting insulin levels decreased by 14%, and HOMA-IR (homeostatic model assessment of insulin resistance) improved significantly, suggesting that the fat loss was accompanied by metabolic benefits beyond aesthetics.

One critical limitation in extrapolating these findings to non-deficient populations: growth hormone secretagogues produce the most dramatic results in individuals with blunted endogenous GH secretion. Aging adults, those with metabolic syndrome, or individuals in chronic caloric deficit with suppressed leptin and thyroid signaling. A healthy 25-year-old with normal GH pulsatility may experience measurable but less pronounced fat loss from hexarelin compared to a 45-year-old with age-related GH decline. The literature consistently shows a dose-response relationship up to approximately 2 mcg/kg; doses above this threshold increase cortisol and prolactin co-release without proportional GH benefit, a phenomenon known as receptor desensitization or ceiling effect.

Real Peptides has worked with research institutions studying GH secretagogue kinetics in metabolic disease models. One consistent observation: hexarelin's fat loss efficacy is amplified when combined with structured resistance training and adequate dietary protein (1.6–2.2 g/kg body weight). The GH pulse elevates circulating free fatty acids, but those fatty acids must be oxidized through energy expenditure. Hexarelin does not increase basal metabolic rate directly. Investigators using hexarelin for fat loss in sedentary models see modest reductions in adiposity; those pairing it with progressive overload training and moderate caloric deficit see body recomposition that exceeds what either intervention produces independently.

Hexarelin vs Other Growth Hormone Secretagogues — Potency and Selectivity

The growth hormone secretagogue class includes multiple peptides with varying receptor selectivity, GH release amplitude, and side effect profiles. Hexarelin for fat loss sits at the high end of potency but also carries the highest risk of cortisol and prolactin co-secretion, particularly at doses exceeding 100 mcg per administration. Ipamorelin, by contrast, is considered the most selective GH secretagogue. It produces robust GH release with minimal cortisol or prolactin elevation, making it preferable for long-term protocols where hypothalamic-pituitary-adrenal (HPA) axis suppression is a concern. GHRP-2 and GHRP-6 fall between hexarelin and ipamorelin in terms of GH amplitude and side effect burden.

Peak GH release following hexarelin administration (2 mcg/kg) typically reaches 15–25 ng/mL in responsive individuals, compared to 8–15 ng/mL with ipamorelin at equivalent dosing. However, hexarelin's prolactin response can elevate plasma prolactin by 30–50% above baseline, which may interfere with dopamine signaling and, in chronic use, contribute to libido suppression or gynecomastia in susceptible males. Ipamorelin produces less than 10% prolactin elevation at therapeutic doses, making it the safer choice for extended fat loss protocols lasting 12+ weeks. For short-term applications (4–6 weeks) where maximal GH output is prioritized, hexarelin's superior potency may justify the trade-off.

Another consideration: receptor desensitization. Chronic daily administration of hexarelin leads to progressive attenuation of GH response over 8–12 weeks, a phenomenon documented in multiple studies. This desensitization appears to result from GHSR-1a receptor downregulation in response to sustained agonist exposure. Cycling protocols. 5 days on, 2 days off, or 4 weeks on, 2 weeks off. Are commonly employed to preserve receptor sensitivity. Ipamorelin exhibits slower desensitization kinetics, likely due to its more selective receptor profile and lower constitutive activity at GHSR-1a.

For researchers and clinicians exploring hexarelin for fat loss, the comparison table below summarizes key pharmacological differences between commonly used GH secretagogues. Real Peptides offers research-grade formulations of all compounds listed, synthesized under USP standards with third-party purity verification available on request.

Hexarelin for Fat Loss: Growth Hormone Secretagogue Comparison

Understanding how hexarelin for fat loss compares to other peptides in the GH secretagogue class is essential for selecting the appropriate compound for specific research or clinical applications. The table below contrasts hexarelin with Ipamorelin, GHRP-2, and GHRP-6 across key pharmacological parameters.

Peptide	Peak GH Release (ng/mL at 2 mcg/kg)	Cortisol Co-Release	Prolactin Co-Release	Receptor Desensitization	Best Use Case	Professional Assessment
Hexarelin	15–25 ng/mL	Moderate (20–30% increase)	High (30–50% increase)	Rapid (8–12 weeks)	Short-term maximal GH output; aggressive fat loss phases	Highest potency but side effect burden limits long-term use. Cycle on/off or reserve for 4–6 week protocols
Ipamorelin	8–15 ng/mL	Minimal (<5% increase)	Minimal (<10% increase)	Slow (16+ weeks)	Long-term body recomposition; maintenance protocols	Most selective profile. Ideal for extended use with minimal HPA disruption
GHRP-2	10–18 ng/mL	Moderate (15–25% increase)	Moderate (20–35% increase)	Moderate (12–16 weeks)	Balanced potency and tolerability; moderate-term fat loss	Middle ground between hexarelin's power and ipamorelin's selectivity
GHRP-6	9–16 ng/mL	Low (10–15% increase)	Low (15–20% increase)	Moderate (12–16 weeks)	Appetite stimulation contexts; joint/connective tissue support	Notable ghrelin-mimetic hunger increase. Less suitable for deficit-driven fat loss

The bottom line: hexarelin for fat loss delivers the highest GH amplitude, making it the most effective secretagogue for rapid adipose reduction in time-sensitive contexts. However, prolactin elevation and faster receptor desensitization mean it is best reserved for short, aggressive phases rather than sustained year-round use. For long-term metabolic management, Ipamorelin offers superior tolerability and sustained efficacy without HPA axis disruption.

What If: Hexarelin for Fat Loss Scenarios

What If I Use Hexarelin for Fat Loss Without Being in a Caloric Deficit?

Hexarelin will still elevate growth hormone and mobilize free fatty acids into circulation, but those fatty acids must be oxidized through energy expenditure to produce net fat loss. If caloric intake matches or exceeds total daily energy expenditure (TDEE), the mobilized fatty acids will be re-esterified and stored in adipose tissue rather than burned for fuel. Growth hormone creates a permissive metabolic environment for lipolysis, but it does not override thermodynamics. Fat oxidation requires a negative energy balance. Research in growth hormone-deficient adults shows that GH replacement without dietary modification produces minimal fat loss despite normalized GH levels, confirming that the hormone facilitates but does not independently drive adipose reduction.

What If Hexarelin for Fat Loss Stops Working After 8 Weeks?

You are likely experiencing GHSR-1a receptor desensitization, a well-documented phenomenon where chronic agonist exposure downregulates receptor density and responsiveness. The solution is a washout period. Discontinue hexarelin for 2–4 weeks to allow receptor upregulation, then resume at the original dose. Alternatively, rotate to a different GH secretagogue like Ipamorelin or GHRP-2 during the washout phase to maintain GH output through a different receptor activation pattern. Some protocols use hexarelin for 4–6 weeks at maximum intensity, then switch to ipamorelin for 8–12 weeks of maintenance, cycling back to hexarelin only when aggressive fat loss is again prioritized.

What If I Experience Elevated Prolactin Symptoms While Using Hexarelin for Fat Loss?

Symptoms such as gynecomastia, libido suppression, or lactation (in females) indicate that prolactin elevation has exceeded physiological tolerance. Discontinue hexarelin immediately and transition to a more selective GH secretagogue like Ipamorelin, which produces less than 10% prolactin elevation at therapeutic doses. In research settings, dopamine agonists such as cabergoline (0.25–0.5 mg twice weekly) are used to suppress prolactin when GH secretagogue protocols cannot be interrupted, but this introduces additional pharmacological complexity and should only be undertaken under medical supervision. Hexarelin's prolactin response is dose-dependent. Reducing dose to 1 mcg/kg or less may eliminate symptoms while preserving partial GH benefit.

The Evidence-Based Truth About Hexarelin for Fat Loss

Here's the honest answer: hexarelin for fat loss works, but it is not a standalone solution, and the marketing claims often exceed what the peer-reviewed literature supports. Yes, it stimulates growth hormone secretion more potently than nearly any other peptide secretagogue. Yes, that GH pulse mobilizes stored triglycerides and elevates circulating free fatty acids. But mobilization is not oxidation. Hexarelin creates the metabolic conditions for fat loss, it does not burn fat directly. Without a caloric deficit and structured training stimulus, the fat loss will be modest at best.

The second reality: hexarelin's side effect profile. Particularly prolactin elevation and receptor desensitization. Limits its suitability for long-term use. It is a sprint tool, not a marathon compound. Researchers and clinicians who achieve the best outcomes with hexarelin for fat loss use it in short, aggressive phases (4–6 weeks) during plateau-breaking interventions, then rotate to more sustainable secretagogues like Ipamorelin or Sermorelin for maintenance. The ceiling effect is real. Doses above 2 mcg/kg do not produce proportionally greater GH release, they just amplify cortisol and prolactin spikes.

Finally, hexarelin is not a substitute for metabolic fundamentals. If thyroid function is suppressed, insulin sensitivity is impaired, or dietary protein is inadequate, no amount of GH pulsatility will produce meaningful body recomposition. The peptide amplifies what is already in place. It does not compensate for poor sleep, inadequate recovery, or haphazard nutrition. Real Peptides works with labs and clinicians who understand this distinction. Hexarelin for fat loss is one tool in a comprehensive metabolic optimization protocol, not a shortcut around foundational work.

Hexarelin sits at the intersection of potent pharmacology and practical limitations. Used correctly. In cycling protocols, paired with resistance training, and embedded within structured deficit phases. It accelerates fat loss beyond what diet and exercise produce independently. Used carelessly. Continuous daily dosing, no training stimulus, caloric surplus. It becomes an expensive placebo with unwanted endocrine side effects. That is not a flaw in the compound; it is a reminder that mechanism and application are equally important.

If you are conducting research into GH secretagogues and metabolic optimization, Hexarelin is available through Real Peptides as a high-purity, lyophilized powder synthesized under strict USP guidelines with third-party verification. For labs seeking broader peptide portfolios for comparative studies, explore our full peptide collection covering growth hormone pathways, metabolic signaling, and body recomposition research.

The most effective hexarelin for fat loss protocols pair short-duration, high-intensity peptide phases with long-term metabolic management using compounds with better side effect profiles. That is not a limitation. It is a blueprint. Understanding when to use hexarelin, when to rotate off, and how to structure the intervention around training and nutrition is what separates meaningful fat loss from expensive disappointment.

References

Peer-reviewed sources on Hexarelin indexed in PubMed, listed for research context. Real Peptides supplies Hexarelin for laboratory research use only.

Hexarelin alleviates apoptosis on ischemic acute kidney injury via MDM2/p53 pathway. European journal of medical research, 2023. PMID 37710348. doi:10.1186/s40001-023-01318-w
Hexarelin attenuates abdominal aortic aneurysm formation by inhibiting SMC phenotype switch and inflammasome activation. Microvascular research, 2022. PMID 34856183. doi:10.1016/j.mvr.2021.104280
Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury. Drug target insights, 2021. PMID 34871336. doi:10.33393/dti.2021.2347
Hexarelin Modulation of MAPK and PI3K/Akt Pathways in Neuro-2A Cells Inhibits Hydrogen Peroxide-Induced Apoptotic Toxicity. Pharmaceuticals (Basel, Switzerland), 2021. PMID 34066741. doi:10.3390/ph14050444
Using Synchrotron Radiation Imaging Techniques to Elucidate the Actions of Hexarelin in the Heart of Small Animal Models. Frontiers in physiology, 2021. PMID 35126171. doi:10.3389/fphys.2021.766818
Ghrelin receptor agonist hexarelin attenuates antinociceptive tolerance to morphine in rats. Canadian journal of physiology and pharmacology, 2021. PMID 32893668. doi:10.1139/cjpp-2020-0218
Hexarelin targets neuroinflammatory pathways to preserve cardiac morphology and function in a mouse model of myocardial ischemia-reperfusion. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2020. PMID 32403043. doi:10.1016/j.biopha.2020.110165
Hexarelin attenuates atherosclerosis via inhibiting LOX-1-NF-κB signaling pathway-mediated macrophage ox-LDL uptake in ApoE(-/-) mice. Peptides, 2019. PMID 31386895. doi:10.1016/j.peptides.2019.170122

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