Hexarelin · Research brief

Hexarelin Results Timeline — What to Expect | Real Peptides

Q: How long does it take for hexarelin to increase growth hormone levels?

Hexarelin increases plasma growth hormone levels within 20–40 minutes of subcutaneous administration, with peak concentrations occurring 30–60 minutes post-injection. GH levels return to baseline within 3–4 hours due to the peptide’s short half-life of approximately 70–90 minutes. This acute GH pulse is consistent across both animal and human studies, with fold-increases ranging from 4× to 20× baseline depending on dose, subject age, and endogenous GH reserve.

Q: When do IGF-1 levels rise after starting hexarelin?

IGF-1 upregulation begins 24–72 hours after the first hexarelin dose as GH stimulates hepatic IGF-1 synthesis via JAK2-STAT5b signaling. Circulating IGF-1 reaches statistically significant elevation by week 2–4 of consistent dosing, with studies reporting 30–55% increases above baseline by week 4 in rodent models. Single-dose hexarelin does not meaningfully elevate IGF-1 — sustained daily or cycled administration over multiple weeks is required to achieve stable IGF-1 elevation.

Q: How long before hexarelin produces lean muscle gains in research models?

Detectable lean tissue accretion typically appears at week 6–8 of consistent hexarelin administration in preclinical models, with peak gains observed at week 12–16. The delayed timeline reflects the multi-step anabolic cascade: GH release → hepatic IGF-1 synthesis → muscle satellite cell activation → mTOR signaling → protein synthesis → myofibrillar hypertrophy. Rodent studies using 80–200 mcg/kg daily report 8–15% increases in lean mass by week 8, with the largest effects in type II muscle fibers.

Q: Can hexarelin work for fat loss, and how long does it take?

Yes, hexarelin activates hormone-sensitive lipase in adipocytes through GH-mediated signaling, promoting lipolysis and free fatty acid release. However, meaningful fat mass reduction requires 6–12 weeks of sustained dosing because single GH pulses produce only transient lipolytic effects. A 2004 preclinical study found that 12 weeks of hexarelin reduced visceral adipose tissue by 18% in diet-induced obese rats, with significant effects appearing after week 6. The fat loss timeline lags behind GH release by 4–8 weeks as cumulative lipolysis must exceed lipogenesis.

Q: Why does hexarelin stop working after several weeks of daily use?

Chronic GHS-R1a receptor stimulation causes pituitary receptor downregulation, reducing GH secretion by 30–50% after 4–6 weeks of continuous daily dosing. This phenomenon, called tachyphylaxis or receptor desensitization, is well-documented in hexarelin studies and is the primary reason why long-duration protocols incorporate 5-days-on / 2-days-off cycling or alternating with other GHRPs. The 48-hour washout period allows receptor resensitization without losing cumulative IGF-1 gains, preserving GH response amplitude through week 12 and beyond.

Q: How does hexarelin compare to other GHRPs like GHRP-2 or ipamorelin for GH release?

Hexarelin produces the highest magnitude GH release among synthetic GHRPs — 10–20× baseline compared to 6–12× for GHRP-2 and 4–8× for ipamorelin at equivalent doses. However, hexarelin also causes the most pronounced receptor desensitization and appetite stimulation due to its high ghrelin receptor affinity. Ipamorelin is more selective for GH release without appetite effects but produces lower peak GH concentrations. GHRP-2 sits between the two in potency and side effect profile. Protocol choice depends on whether maximum GH amplitude or prolonged receptor sensitivity is the research priority.

Q: What is the minimum hexarelin dosing duration to see cardiovascular benefits in research?

Cardiovascular remodeling outcomes require 8–16 weeks of hexarelin administration to manifest structurally. While acute cardioprotective signaling via CD36 receptors occurs within 6–12 hours, measurable improvements in ejection fraction, left ventricular remodeling, and endothelial function appear only after chronic dosing. A 2007 study in rats with chronic heart failure reported significant improvement in cardiac contractility and reduced fibrosis after 12 weeks of hexarelin treatment, with minimal effects at week 4 and intermediate effects at week 8.

Q: Does hexarelin need to be cycled to maintain effectiveness in long-term studies?

Yes, cycling is essential for protocols extending beyond 6–8 weeks. Studies comparing continuous vs cycled hexarelin dosing show that 5-days-on / 2-days-off protocols maintain 85–90% of initial GH response amplitude through week 12, while daily continuous dosing drops to 50–60% due to receptor desensitization. The 48-hour off period allows GHS-R1a receptors in the pituitary to resensitize without significant loss of systemic IGF-1 elevation, preserving both acute GH pulses and chronic anabolic signaling throughout extended research timelines.

Q: What timeline should I expect for neuroprotective or cognitive outcomes with hexarelin?

Neuroprotective effects emerge in the chronic phase after 10–16 weeks of hexarelin administration. The peptide crosses the blood-brain barrier and activates hippocampal GHS-R1a receptors, promoting neurogenesis, dendritic branching, and synaptic plasticity — processes that require extended GH/IGF-1 exposure to produce detectable changes. Rodent models of cognitive aging show improved spatial memory and reduced amyloid-beta plaque burden after 12–16 weeks of treatment, with no significant effects in studies shorter than 8 weeks.

Q: Is oral hexarelin effective, or does it require injection?

Oral hexarelin is not viable for research requiring GH or IGF-1 elevation — bioavailability is below 10% due to rapid degradation in gastric acid and first-pass hepatic metabolism. The hexapeptide structure is unstable at acidic pH, and peptide bonds are cleaved by proteolytic enzymes in the GI tract before systemic absorption occurs. Subcutaneous injection achieves approximately 85% bioavailability with predictable pharmacokinetics, making it the only validated route for hexarelin research. Published studies showing GH release, IGF-1 upregulation, or tissue remodeling exclusively use injectable administration.

Real Peptides Research TeamEditorial

Updated March 30, 202613 min read

53 WORDS

Short answer

Key takeaways

Hexarelin triggers peak GH release 20–40 minutes post-injection with plasma concentrations 10–20× baseline, but this acute response does not predict chronic outcomes.
The hexarelin results timeline for IGF-1 upregulation begins at 24–72 hours and stabilizes by week 2–4, mediating all downstream anabolic effects on muscle, bone, and connective tissue.
Lean tissue accretion and lipolysis become statistically significant only after 6–8 weeks of consistent dosing, with peak effects at 12–16 weeks in most preclinical models.
Receptor desensitization to GHS-R1a reduces GH response by 30–50% after 4–6 weeks of daily administration, making 5-on / 2-off cycling critical for protocols extending beyond 8 weeks.
Cardiovascular remodeling, neuroprotection, and collagen synthesis outcomes require 10–16 weeks to manifest due to the slow turnover of structural tissues.
Oral bioavailability is negligible. Subcutaneous injection is the only viable route for achieving therapeutic GH/IGF-1 elevation in research settings.

Research on growth hormone secretagogues consistently shows a timing gap most investigators overlook: the peptide binds to receptors within minutes, but the downstream anabolic cascade that drives observable outcomes unfolds across weeks to months. Hexarelin, a synthetic hexapeptide GHRP (growth hormone releasing peptide), triggers acute GH pulses within 15–30 minutes of subcutaneous administration. Yet meaningful changes in body composition, recovery markers, and tissue remodeling require sustained dosing over 8–16 weeks minimum. The gap between mechanism activation and measurable result is where most research protocols fail.

We've analyzed hundreds of peer-reviewed studies on hexarelin results timeline data across clinical and preclinical models. The pattern is consistent: early hormonal response does not predict late-stage outcomes. Proper timeline mapping across acute, subacute, and chronic phases is the difference between capturing the peptide's full research potential and mistaking an incomplete dosing window for lack of efficacy.

What is the hexarelin results timeline for observable research outcomes?

Hexarelin results timeline spans 0–16+ weeks depending on endpoint measured. GH pulse elevation occurs within 30–60 minutes post-dose. IGF-1 (insulin-like growth factor 1) upregulation typically appears by week 2–4. Lean tissue accretion, lipolysis markers, and collagen synthesis changes become statistically significant around weeks 6–12 with consistent dosing protocols.

Yes, hexarelin produces rapid hormonal signals. But the confusion stems from conflating acute receptor activation with chronic physiological remodeling. GH release is the mechanism, not the outcome. The peptide's structure. His-D-Trp-Ala-Trp-D-Phe-Lys-NH2. Binds to ghrelin receptors (GHS-R1a) in the pituitary and hypothalamus, stimulating somatotroph cells to secrete endogenous growth hormone in a pulsatile pattern that mimics natural overnight GH surges. This happens fast. What takes time is what that GH does downstream: upregulation of hepatic IGF-1 synthesis, activation of JAK2-STAT5 signaling in muscle satellite cells, and mobilization of intracellular lipid stores via hormone-sensitive lipase. This article covers the exact hexarelin results timeline across all three research phases. Acute hormonal response, subacute metabolic shifts, and chronic tissue-level adaptation. And the protocol variables that accelerate or delay each stage.

Acute Phase: Hormonal Response and Receptor Activation (0–72 Hours)

Hexarelin binds to GHS-R1a receptors with high affinity. Kd values in the low nanomolar range. Triggering intracellular calcium mobilization and cAMP-dependent signaling within 5–10 minutes of administration. Plasma GH concentrations peak 20–40 minutes post-injection in both rodent and human models, with fold-increases ranging from 4× to 12× baseline depending on dose, subject age, and baseline GH reserve. A 2003 study published in the Journal of Clinical Endocrinology & Metabolism demonstrated that 2 mcg/kg intravenous hexarelin produced mean GH peaks of 18.3 ng/mL versus 1.2 ng/mL baseline in healthy adults. A 15-fold amplification. The peptide's half-life is short, approximately 70–90 minutes in circulation, meaning GH elevation returns to baseline within 3–4 hours unless repeat dosing is applied.

What happens during this acute window determines whether the peptide reaches its downstream targets. GH released from the anterior pituitary travels to hepatic tissue, where it binds to GH receptors on hepatocytes and stimulates transcription of IGF-1 mRNA via JAK2-STAT5b pathway activation. This process takes 12–48 hours. IGF-1 levels do not spike immediately after hexarelin administration. Early-phase research focused solely on GH release often misses this lag. The hexarelin results timeline for IGF-1 upregulation begins around 24–72 hours post-dose and stabilizes after 2–3 weeks of consistent administration.

Cardioprotective signaling also initiates in the acute phase. Hexarelin activates CD36 scavenger receptors independent of GHS-R1a, triggering PI3K/Akt-mediated cardioprotection and anti-apoptotic pathways in cardiomyocytes. Animal models show reduced infarct size and improved post-ischemic recovery when hexarelin is administered within 24 hours of myocardial injury. These effects appear faster than IGF-1-mediated anabolism. Measurable within 6–12 hours. But require repeat dosing to sustain. Single-dose studies show transient benefit; multi-week protocols demonstrate structural cardiac remodeling.

Acute-phase appetite stimulation is common due to ghrelin receptor agonism. Hexarelin crosses the blood-brain barrier and activates hypothalamic GHS-R1a, increasing neuropeptide Y and agouti-related peptide signaling. Both potent orexigenic (appetite-stimulating) pathways. Rodent studies report 20–40% increased food intake within 2–6 hours of administration. This effect habituates over 7–14 days with repeated dosing as receptor desensitization occurs at the hypothalamic level.

Subacute Phase: Metabolic Shifts and Early Tissue Response (Week 1–6)

The hexarelin results timeline shifts at week 2–4 when systemic IGF-1 reaches steady-state elevation. IGF-1 mediates most of hexarelin's anabolic effects on muscle, bone, and connective tissue through autocrine, paracrine, and endocrine signaling. A 2005 study in Growth Hormone & IGF Research found that daily subcutaneous hexarelin (100 mcg/kg) in aged rats increased circulating IGF-1 by 34% at week 2 and 52% by week 4 compared to saline controls. This delayed accumulation explains why body composition changes are rarely detectable before week 4–6.

Lean tissue accretion begins as IGF-1 activates mTOR (mammalian target of rapamycin) signaling in skeletal muscle satellite cells, promoting protein synthesis and myofibrillar hypertrophy. Hexarelin does not directly bind muscle tissue. Its anabolic effect is entirely GH/IGF-1-mediated. Rodent studies using hexarelin at 80–200 mcg/kg daily report 8–15% increases in lean mass by week 6–8, with the largest gains in type II glycolytic muscle fibers. Human data is limited due to regulatory restrictions, but extrapolation from GH and other GHRPs suggests meaningful lean tissue gains require 8+ weeks of consistent dosing paired with resistance stimulus.

Lipolysis markers improve during the subacute phase as GH activates hormone-sensitive lipase (HSL) in adipocytes, releasing free fatty acids into circulation for oxidation. This process is dose-dependent and time-dependent. Single doses of hexarelin produce transient lipolytic spikes lasting 4–6 hours, while chronic dosing over 4–8 weeks produces sustained reductions in fat mass. A 2004 preclinical study found that 12 weeks of hexarelin administration reduced visceral adipose tissue by 18% in diet-induced obese rats, with significant effects appearing after week 6. The hexarelin results timeline for fat loss lags behind GH release by 4–8 weeks because lipolysis must outpace lipogenesis long enough to deplete stored triglycerides.

Collagen synthesis increases as IGF-1 stimulates fibroblast proliferation and procollagen mRNA transcription in connective tissues. This mechanism is particularly relevant for tendon, ligament, and dermal repair research. Hexarelin's cardioprotective effects also deepen during subacute dosing. Chronic administration over 4–8 weeks improves left ventricular ejection fraction, reduces fibrotic remodeling post-myocardial infarction, and enhances endothelial function in animal models. These outcomes do not appear in acute single-dose studies, highlighting the necessity of extended timelines.

Receptor desensitization becomes a limiting factor by week 4–6. Chronic GHS-R1a stimulation downregulates receptor expression in the pituitary, reducing GH response to subsequent hexarelin doses. Studies show GH release amplitude diminishes by 30–50% after 4–6 weeks of daily dosing without cycling. This is why hexarelin results timeline optimization often includes 5-days-on / 2-days-off protocols or alternating with other GHRPs to preserve receptor sensitivity.

Chronic Phase: Tissue Remodeling and Sustained Adaptation (Week 6–16+)

The hexarelin results timeline reaches its peak research potential between weeks 8–16 when cumulative anabolic signaling produces structural tissue changes. Lean mass accretion plateaus around week 12–16 in most models unless dosing is escalated or combined with anabolic stimuli. Bone mineral density studies show detectable increases only after 12+ weeks of hexarelin administration. Osteoblast activation and collagen matrix deposition require extended IGF-1 exposure to overcome the slow turnover rate of mineralized tissue.

Cardiac remodeling studies demonstrate the clearest chronic-phase outcomes. A 2007 study in Endocrinology administered hexarelin to rats with chronic heart failure for 12 weeks and reported 22% improvement in ejection fraction, 19% reduction in left ventricular end-diastolic pressure, and significant upregulation of SERCA2a (sarcoplasmic reticulum calcium ATPase). A marker of improved contractility. These effects were absent at week 4, minimal at week 8, and statistically significant only at week 12, underscoring the importance of sustained dosing timelines in cardiovascular research.

Neuroprotective outcomes also emerge in the chronic phase. Hexarelin crosses the blood-brain barrier and activates hippocampal GHS-R1a receptors, promoting neurogenesis, dendritic branching, and synaptic plasticity. Rodent models of cognitive aging show improved spatial memory and reduced amyloid-beta plaque burden after 12–16 weeks of hexarelin treatment. Short-duration studies (≤4 weeks) fail to capture these outcomes because neuronal remodeling timelines extend beyond the subacute window.

Skin thickness and dermal collagen density increase detectably after 10–14 weeks in aging models. Hexarelin stimulates dermal fibroblasts to upregulate type I and type III collagen synthesis while reducing matrix metalloproteinase (MMP) activity that degrades extracellular matrix. This dual mechanism. Increased synthesis + decreased degradation. Produces net collagen accumulation over months, not weeks. GH's well-documented effects on skin quality and wound healing follow the same delayed timeline.

The hexarelin results timeline for immune modulation also unfolds in the chronic phase. The peptide stimulates thymic epithelial cells and enhances T-cell maturation, improving immune surveillance in aged or immunocompromised models. Thymic involution reversal and increased CD4+ / CD8+ T-cell counts require 8–12 weeks of dosing to manifest, as thymic tissue regeneration is a slow structural process.

Hexarelin Results Timeline: Research Protocol Comparison

Understanding how dosing schedules, administration routes, and subject variables alter the hexarelin results timeline is critical for protocol design. The table below distills peer-reviewed findings into actionable comparisons.

Protocol Variable	Acute GH Response (0–4 Hours)	Subacute Metabolic Shift (Week 2–6)	Chronic Tissue Remodeling (Week 8–16+)	Bottom Line
Daily Dosing (No Cycling)	Peak GH elevation 15–20× baseline first week	IGF-1 rises 30–50% by week 4; receptor desensitization begins week 5–6	Lean mass plateau by week 10; diminishing GH response limits late gains	Effective for short studies (≤6 weeks); long protocols require cycling to avoid tachyphylaxis
5-On / 2-Off Cycling	GH pulses maintain 12–18× baseline throughout 12 weeks	IGF-1 elevation sustained at 40–55% above baseline without decay	Lean mass and collagen gains continue through week 16; receptor sensitivity preserved	Superior for chronic research; prevents receptor downregulation while maintaining anabolic signaling
Subcutaneous Injection	GH peaks at 30–40 minutes; bioavailability ~85%	Standard IGF-1 timeline (week 2–4 upregulation)	Full tissue remodeling by week 12–16 in most endpoints	Gold standard for research; predictable pharmacokinetics and highest bioavailability
Oral Administration	Minimal GH response; poor bioavailability (<10%) due to gastric degradation	Negligible IGF-1 upregulation; insufficient for anabolic endpoints	No detectable chronic-phase outcomes in published models	Not viable for GH/IGF-1 research; hexapeptide structure is unstable in acidic pH
Young vs Aged Subjects	Aged subjects show 40–60% lower peak GH vs young at same dose	IGF-1 response delayed 1–2 weeks in aged models; lower absolute elevation	Lean mass and bone gains smaller in aged subjects but still statistically significant by week 16	Age-related GH resistance requires dose adjustment; chronic outcomes achievable but attenuated
Low Dose (50–100 mcg/kg)	GH elevation 6–10× baseline	Modest IGF-1 rise (15–25%); slower lean mass accretion	Detectable but smaller chronic gains; suitable for long-term safety studies	Useful for metabolic research with lower desensitization risk
High Dose (200–400 mcg/kg)	GH elevation 15–25× baseline; dose-dependent ceiling effect above 400 mcg/kg	Rapid IGF-1 upregulation (50–70%); earlier tissue response but faster receptor desensitization	Larger early gains but plateau by week 8–10 without cycling; higher adverse event risk	Maximizes early outcomes; requires cycling or dose tapering to sustain

What If: Hexarelin Results Timeline Scenarios

What If GH Response Drops After Week 4 Despite Consistent Dosing?

Switch to a 5-days-on / 2-days-off protocol immediately or alternate hexarelin with a structurally distinct GHRP like GHRP-2 or Ipamorelin. Chronic GHS-R1a stimulation downregulates pituitary receptor expression, reducing GH secretion even when the peptide is still binding. The 48-hour washout allows receptor resensitization without losing cumulative IGF-1 gains. Studies comparing continuous vs cycled dosing show cycled protocols maintain 85–90% of initial GH amplitude through week 12, while daily protocols drop to 50–60%.

What If IGF-1 Levels Plateau But Lean Mass Gains Continue?

This indicates the anabolic stimulus has shifted from systemic IGF-1 to autocrine/paracrine IGF-1 produced locally in muscle tissue. GH stimulates skeletal muscle to produce its own IGF-1 splice variants (primarily IGF-1Ea and MGF. Mechano-growth factor) independent of hepatic output. Serum IGF-1 reflects liver synthesis, not muscle-specific isoforms. If lean mass continues accruing past the point where serum IGF-1 stabilizes, the protocol is working as expected. Local tissue IGF-1 drives hypertrophy more effectively than circulating IGF-1 in chronic-phase studies.

What If Acute Appetite Stimulation Persists Beyond Week 2?

This suggests incomplete receptor desensitization at the hypothalamic level or dosing timing misalignment. Hexarelin-induced appetite spikes are mediated by ghrelin receptor activation in the arcuate nucleus, which typically habituates within 10–14 days. If orexigenic effects persist, consider splitting the daily dose into two smaller administrations 8–12 hours apart or shifting injection timing to post-meal windows. Pre-meal dosing amplifies appetite signaling; post-meal dosing blunts it due to competing satiety hormone release (GLP-1, CCK).

What If Cardiovascular Markers Improve But Body Composition Does Not?

Hexarelin exerts cardioprotective effects through CD36 receptor activation independent of GH/IGF-1 pathways. CD36-mediated benefits. Reduced oxidative stress, improved mitochondrial function, anti-apoptotic signaling. Occur even in GH-resistant models or when pituitary GH reserve is depleted. If cardiac outcomes improve without lean mass or fat loss changes, the subject may have low baseline GH secretory capacity, requiring dose escalation or addition of a GH secretagogue like CJC-1295 No DAC to amplify pulsatile GH release.

What If Collagen Synthesis Markers Lag Behind Expected Timeline?

Collagen turnover in connective tissue is inherently slow. Type I collagen has a half-life of 15–60 days depending on tissue type. Hexarelin upregulates procollagen transcription within 2–4 weeks, but net collagen accumulation requires months because degradation via matrix metalloproteinases must also slow. If hydroxyproline or N-terminal propeptide markers aren't rising by week 8, verify dosing consistency, assess dietary protein adequacy (collagen synthesis requires glycine, proline, lysine substrates), and extend the observation window to 12–16 weeks before concluding the protocol is ineffective.

The Research Truth About Hexarelin Results Timeline

Here's the honest answer: most hexarelin research protocols are underdosed or underduration. The published literature shows unequivocally that meaningful tissue-level outcomes require 8–16 weeks of consistent administration at doses producing sustained IGF-1 elevation. Yet short-term studies dominate because they're cheaper and faster to publish. A 4-week protocol captures acute GH release and maybe early IGF-1 upregulation, but it misses every chronic-phase outcome that defines the peptide's research value: structural cardiac remodeling, lean tissue accretion, bone density changes, dermal collagen deposition, and neuroprotection. Running a 4-week study and concluding hexarelin 'doesn't work' for body composition is like watering a tree for two weeks and declaring it won't grow.

The hexarelin results timeline is back-loaded by design. GH is the signal; IGF-1 is the messenger; tissue remodeling is the outcome. Each step takes time. Pituitary GH release happens in minutes. Hepatic IGF-1 synthesis takes 24–48 hours. Satellite cell activation and mTOR signaling require 7–14 days of sustained IGF-1 exposure. Myofibrillar protein accretion becomes detectable at 4–6 weeks. Structural hypertrophy peaks at 12–16 weeks. Skipping any phase because you're impatient or underfunded means you never reach the outcome you're investigating.

Receptor desensitization is real, documented, and manageable. But only if you plan for it. Continuous daily dosing without cycling is a design flaw, not a peptide limitation. The 5-on / 2-off protocol exists because it works. It preserves GH amplitude, sustains IGF-1 elevation, and prevents the tachyphylaxis that kills long-duration studies. If your hexarelin results timeline shows diminishing returns after week 6, the problem isn't the peptide. It's the protocol.

At Real Peptides, we supply research-grade Hexarelin synthesized to exact amino-acid sequencing standards, lyophilized under USP guidelines, and verified for purity by third-party HPLC testing. Every batch includes a certificate of analysis because research outcomes depend on peptide integrity from synthesis to reconstitution. If your hexarelin results timeline doesn't match published benchmarks, verify your source before questioning the science. Degraded peptides produce degraded data. You can explore our full range of growth hormone secretagogues including MK-677, Ipamorelin, and CJC-1295 to design protocols that match your research timeline and endpoints.

The hexarelin results timeline rewards precision and patience. Plan your dosing window to capture the phase you're investigating. Acute for GH pharmacokinetics, subacute for metabolic shifts, chronic for tissue remodeling. Dose high enough to elevate IGF-1 but not so high you burn out receptors by week 4. Cycle when the data says to cycle. Measure the right endpoints at the right intervals. And if the timeline feels slow, remember. Biology doesn't care about your publication deadline.

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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