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Sermorelin

5mg Vial
10mg Vial
2 September 2026Updated 2 September 2026
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Full range of benefits for Sermorelin

Stimulates endogenous growth hormone release from the anterior pituitary

Can increase circulating IGF-1 levels, a mediator of GH effects

May support increases in lean muscle mass and strength

May aid reduction of fat mass, particularly visceral adiposity

May improve sleep quality and sleep architecture

May enhance exercise recovery and tissue repair

May help maintain or improve bone mineral density over time

May improve skin thickness and collagen synthesis

Promotes physiological, pulsatile GH secretion versus continuous GH

Short peptide with a relatively short half-life, enabling titration

Stimulating endogenous GH tends to limit prolonged supraphysiologic GH levels

Used in diagnostic testing for pituitary growth hormone reserve

This peptide's combination-safety and interaction data below always stays visible, regardless of membership.

Warning

Important information. The data compiled from scientific literature is provided for educational purposes. Dosage ranges reflect what is reported in studies and do not constitute a recommendation, prescription, or usage guidance. Health decisions should always be made with a qualified professional.

Peptide Interactions

// 13 known interactions

Not recommended for concurrent use

Oral estrogens (e.g., ethinyl estradiol, oral contraceptives)

Oral estrogen administration can reduce hepatic IGF-1 production and blunt the biochemical response to GHRH analogues, so benefits and dosing should be carefully evaluated.

Somatostatin analogues (e.g., octreotide, lanreotide)

Somatostatin analogues directly inhibit GH secretion and may antagonize the effect of sermorelin, so co-prescription should be carefully justified and reviewed.

Antipsychotics (dopamine antagonists, e.g., risperidone)

Dopamine antagonists can elevate prolactin and perturb hypothalamic regulation of GH, and they carry metabolic risk that may complicate sermorelin therapy, warranting careful evaluation.

All interaction categories

Synergistic (3)

  • GHRP-6: A ghrelin-receptor agonist that acts via a complementary pathway to GHRH, producing additive stimulation of pulsatile GH secretion when combined with sermorelin.
  • Ipamorelin: A selective ghrelin-mimetic GH secretagogue that synergizes with GHRH analogues like sermorelin to increase amplitude of GH pulses with relatively low ACTH/cortisol stimulation.
  • Testosterone (replacement therapy): Testosterone replacement has anabolic effects that can be additive to GH/IGF-1–mediated increases in lean body mass and bone density when used alongside sermorelin.

Compatible (3)

  • Statins (e.g., atorvastatin): Lipid-lowering statins have no direct antagonistic interaction with sermorelin and are generally neutral in co-administration from a GH-axis perspective.
  • ACE inhibitors (e.g., lisinopril): Antihypertensive ACE inhibitors do not substantially alter GH secretion and are typically compatible with sermorelin therapy without special adjustments.
  • Vitamin D (cholecalciferol) and calcium supplements: Bone-supportive supplementation is generally neutral and can be continued with sermorelin to support skeletal health without direct pharmacologic interaction.

Monitor (4)

  • Insulin and oral antidiabetic agents (e.g., metformin, sulfonylureas): Sermorelin–induced increases in GH/IGF-1 can alter glucose metabolism and insulin sensitivity, so glycaemic control and antidiabetic dosing should be monitored and adjusted as needed.
  • Exogenous human growth hormone (somatropin) or IGF-1 therapy: Concomitant use increases risk of excessive GH/IGF-1 effects (edema, arthralgia, insulin resistance), so IGF-1 levels and clinical signs require close monitoring if combined.
  • Levothyroxine (thyroid hormone replacement): Thyroid status influences GH responsiveness and metabolism, so thyroid function tests and potential levothyroxine dose adjustments should be monitored during sermorelin therapy.
  • Systemic glucocorticoids (e.g., prednisone): Glucocorticoids antagonize GH action and can blunt GH release, necessitating monitoring of clinical response and potential dose/timing adjustments of either therapy.

Avoid (3)

  • Oral estrogens (e.g., ethinyl estradiol, oral contraceptives): Oral estrogen administration can reduce hepatic IGF-1 production and blunt the biochemical response to GHRH analogues, so benefits and dosing should be carefully evaluated.
  • Somatostatin analogues (e.g., octreotide, lanreotide): Somatostatin analogues directly inhibit GH secretion and may antagonize the effect of sermorelin, so co-prescription should be carefully justified and reviewed.
  • Antipsychotics (dopamine antagonists, e.g., risperidone): Dopamine antagonists can elevate prolactin and perturb hypothalamic regulation of GH, and they carry metabolic risk that may complicate sermorelin therapy, warranting careful evaluation.