This reference collects what is documented about research peptides used alongside common prescription medications. It is organized by peptide class, because compounds within a class share the mechanism that drives the interaction.
Read the evidence column carefully. For the metabolic compounds there is real clinical trial data. For repair and nootropic peptides there is essentially none in humans, and every entry is inference from preclinical work. An empty interaction record means nobody has studied the pair, not that the pair is safe.
These compounds slow gastric emptying, so the main consideration is timing of oral medication absorption rather than direct pharmacological conflict.
Swipe the table sideways to see every column.
| Medication | Signal | What is known | Evidence |
|---|---|---|---|
| Metformin | No documented interaction | Complementary metabolic pathways. Combined safely in the SURPASS trial program. | SURPASS-2, NEJM 2021 |
| Insulin and sulfonylureas | Moderate — discuss with a professional | Additive glucose-lowering effect. Clinical programs reduced background doses when combining. | FDA label |
| Warfarin | Low — worth noting | Delayed gastric emptying may shift absorption timing. No direct pharmacological interaction. | FDA label |
| Levothyroxine | Low — worth noting | Absorption timing may shift with slowed gastric emptying. | FDA label |
| SSRIs and SNRIs | No documented interaction | The incretin pathway does not meaningfully cross serotonergic pathways. | Clinical practice data |
| Statins | No documented interaction | Separate pathways (incretin signaling vs. HMG-CoA reductase). | Clinical practice data |
No human drug-interaction trials exist for this class. Everything below is extrapolated from preclinical work and should be treated as provisional.
Swipe the table sideways to see every column.
| Medication | Signal | What is known | Evidence |
|---|---|---|---|
| NSAIDs | No documented interaction | Preclinical models show BPC-157 mitigating NSAID-induced gastric injury rather than conflicting with it. | Preclinical (rodent) |
| Corticosteroids | Low — worth noting | Corticosteroids suppress the healing pathways these peptides are studied for; effects may oppose each other. | Mechanistic inference |
| Anticoagulants | Low — worth noting | Angiogenic activity in preclinical models; no human data on bleeding risk. | Preclinical |
| Antibiotics | No documented interaction | No documented interaction in available literature. | No documented data |
These raise endogenous GH and IGF-1. The relevant interactions involve glucose handling and anything else acting on the GH axis.
Swipe the table sideways to see every column.
| Medication | Signal | What is known | Evidence |
|---|---|---|---|
| Exogenous HGH | Moderate — discuss with a professional | Redundant stimulation of the same axis. Combined effects on IGF-1 are additive. | Mechanistic |
| Insulin and diabetes medication | Moderate — discuss with a professional | GH elevation can reduce insulin sensitivity, which may offset glycemic control. | Endocrinology literature |
| Corticosteroids | Low — worth noting | Chronic corticosteroid use blunts GH response. | Endocrinology literature |
| Testosterone | No documented interaction | Different receptor systems; no documented conflict. | Clinical practice data |
Both modulate BDNF and monoamine signaling in preclinical models, which is where the caution with psychiatric medication comes from.
Swipe the table sideways to see every column.
| Medication | Signal | What is known | Evidence |
|---|---|---|---|
| SSRIs and SNRIs | Low — worth noting | Overlapping monoamine modulation in preclinical work. No human interaction studies. | Preclinical |
| Benzodiazepines | Low — worth noting | Selank is studied as an anxiolytic; overlapping effects are plausible but unquantified in humans. | Preclinical |
| Bupropion | Low — worth noting | Both affect dopaminergic tone in preclinical models. | Preclinical |
Interaction data is sparse. The clearest signals are immunomodulation and blood-pressure effects.
Swipe the table sideways to see every column.
| Medication | Signal | What is known | Evidence |
|---|---|---|---|
| Immunosuppressants | Moderate — discuss with a professional | Thymosin Alpha-1 stimulates T-cell activity, which directly opposes immunosuppressive therapy. | Mechanistic |
| Blood pressure medication | Moderate — discuss with a professional | PT-141 produces transient blood pressure changes in clinical studies. | Clinical trial data |
| Metformin | No documented interaction | MOTS-c acts through AMPK, similar to metformin; effects appear complementary in preclinical models. | Preclinical |
"No documented interaction" means the pair has been looked at and nothing meaningful was found, or the mechanisms are clearly separate. "Low" flags something worth mentioning to a prescriber, usually a timing or absorption question rather than a pharmacological conflict. "Moderate" marks pairs where the two agents act on the same system and the combined effect is real enough to need supervision, such as additive glucose lowering or opposing immune effects.
Metabolic compound entries draw on published trial programs and FDA labeling for the corresponding clinical formulations. Entries for repair, nootropic, and immune peptides come from preclinical literature and mechanistic reasoning, and are labeled that way in the evidence column. We deliberately did not fill gaps with plausible-sounding guesses; pairs with no data simply are not listed.
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