Hemopressin (Hp)
The first peptide found to act on the CB1 cannabinoid receptor — curbing appetite and pain without the reward effects of synthetic blockers. A research peptide, not a drug
Hemopressin (Hp) is an unusual peptide: it is cut not from a dedicated signalling-peptide gene but from hemoglobin, the oxygen-carrying protein of red blood cells. A short nine-amino-acid fragment of hemoglobin's alpha chain, it made headlines in 2007 as the first peptide ever shown to bind the CB1 cannabinoid receptor — the same receptor that THC and the body's own endocannabinoids act on, but which until then had only known fatty (lipid) ligands. Hemopressin behaves as a brake on CB1: an antagonist and inverse agonist that switches off the receptor's activity. Through this it reduces food intake (making it a lead against obesity) and relieves pain, including inflammatory and nerve-injury pain. Intriguingly, brain-imaging work suggests it acts on the satiety and pain circuits without hitting the reward centres that caused the psychiatric side effects of synthetic CB1 blockers like rimonabant. N-terminally extended relatives (RVD- and VD-hemopressin, the 'pepcans') round out this hemoglobin-derived cannabinoid-peptide family, and there is scientific debate over whether hemopressin is a genuine endogenous peptide or a fragment formed from the longer one during extraction. Hemopressin is studied as a research tool and a drug lead; it is not an approved medicine and has not been given to people as a treatment.
No established human dose Details ↓
Recommended Dosing
No established human dose
Hemopressin is a hemoglobin-derived peptide that has never been given to people as a treatment. The work is in animals and cells, where hemopressin is given orally or by injection at experimental amounts that do not carry over to people.
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What is it?
The CB1 cannabinoid receptor sits at the centre of the body's endocannabinoid system, controlling appetite, pain, mood and reward. For a long time its only known natural ligands were fatty molecules (the endocannabinoids anandamide and 2-AG). In 2007 researchers screening brain and fat-tissue peptides found the first peptide that binds CB1: hemopressin, a nine-amino-acid fragment of the alpha chain of hemoglobin. That a piece of the blood's oxygen-carrier should act on a brain receptor was a surprise, and it opened a new class of 'peptide cannabinoids'.
Hemopressin acts as a brake on CB1. It selectively blocks signalling by CB1 (but not the related CB2 receptor or other G-protein-coupled receptors) and behaves as an inverse agonist — it damps the receptor's constitutive activity as effectively as the well-known synthetic blocker rimonabant. Structural studies by NMR and molecular docking show the central portion of the peptide forms turn structures critical for fitting the receptor, and a short N-terminal fragment keeps much of the activity.
Because switching CB1 off curbs appetite, hemopressin reduces food intake. Given into the brain or even by mouth, it decreases night-time eating in normal rats and mice and in obese mice, blocks the overeating that a CB1 agonist causes, and has no effect in CB1-knockout animals — strong evidence it works through the receptor. Crucially, brain-imaging work shows it activates the feeding-control nuclei of the hypothalamus and the pain-processing regions of the brainstem, but spares the reward centres (ventral tegmental area, nucleus accumbens) that synthetic CB1 blockers over-dampened — the toxicity that forced rimonabant off the market. This 'satiety not reward' profile is what makes hemopressin interesting.
Hemopressin is also analgesic. It produces antinociception in inflammatory pain and, given by mouth, inhibits neuropathic pain in nerve-injured rats, acting locally through CB1, peripheral potassium channels and the release of the endocannabinoid anandamide. Its longer relatives, RVD-hemopressin (pepcan-12) and VD-hemopressin, behave differently — RVD-hemopressin is a negative allosteric modulator of CB1 while VD-hemopressin can act as an agonist — and some researchers argue that the short hemopressin is actually generated from these longer peptides during tissue extraction, a debate still being resolved.
Hemopressin is a hemoglobin-derived research peptide and a CB1 drug lead, not a medicine. No published study has given hemopressin to people as a treatment — the work is in animals and cells — it is approved nowhere, and material sold online as 'hemopressin' is an unregulated research chemical. Nothing here is a dose or a therapy; this page records what the published science says about the peptide.
Mechanism of Action
Hemopressin is a hemoglobin-derived nonapeptide and the first peptide ligand of the CB1 cannabinoid receptor, acting as an antagonist/inverse agonist. Through CB1 it reduces food intake and relieves inflammatory and neuropathic pain, apparently sparing the brain's reward circuits.
CB1 inverse agonism
Hemopressin selectively binds CB1 (not CB2) and blocks its signalling and constitutive activity as effectively as rimonabant (PMID 18077343); its central turn structures drive the fit (PMID 21062041).
Appetite suppression (satiety, not reward)
By switching CB1 off, hemopressin reduces food intake in normal and obese rodents and blocks CB1-agonist overeating (PMID 20505104), activating hypothalamic satiety circuits while sparing reward centres (PMID 23542442).
Antinociception
Hemopressin relieves inflammatory and neuropathic pain via local CB1 action, peripheral potassium channels and anandamide release (PMIDs 18077343, 24703998).
Published Research
These are studies of hemopressin read from their PubMed abstracts on November 6, 2026. They include the discovery of hemopressin as a CB1 inverse agonist, a review of hemopressin peptides as endocannabinoid-system modulators, animal studies of its reduction of food intake and of neuropathic pain, a brain-imaging study of its central (satiety-not-reward) action, and a structural study of its binding to CB1. Hemopressin has not been given to people as a treatment in any published study; the evidence is animal and cell work.
Hemopressin is a CB1 inverse agonist (discovery)
Screening endogenous peptides for CB1 ligands identified hemopressin (PVNFKFLSH) as a peptide that selectively binds CB1 but not CB2 or other family-A receptors. It is a CB1 antagonist and inverse agonist — blocking signalling and damping the receptor's constitutive activity as well as rimonabant — and in rodent pain models it was antinociceptive by intrathecal, intraplantar and oral routes. The first peptide ligand for CB1, with analgesic potential (a receptor pharmacology study).
Hemopressin peptides as endocannabinoid modulators
A review of hemopressin and its N-terminally extended forms (VD- and RVD-hemopressin) as modulators of the endocannabinoid system. Hemopressin, cut from the hemoglobin alpha chain, acts as a negative modulator of CB1 with antinociceptive, hypophagic and hypotensive effects, though the review notes the debate over whether it is a genuine neuromodulator or a degradation fragment of the longer RVD-hemopressin formed during extraction — and surveys therapeutic prospects for the family.
Hemopressin reduces food intake via CB1
The nonapeptide hemopressin dose-dependently decreased night-time food intake in normal rats and mice and in obese ob/ob mice, whether given centrally or systemically, without obvious side effects. It preserved the normal satiety sequence but attenuated refeeding, blocked CB1-agonist-induced overeating, and had no effect in CB1-knockout mice — strong evidence that hemopressin acts as a functional CB1 antagonist on appetite pathways (a preclinical result).
Hemopressin inhibits neuropathic pain in rats
Oral hemopressin inhibited mechanical hyperalgesia for up to 6 hours in rats with sciatic-nerve injury and reduced a pain-signalling marker in the spinal cord. The effect was independent of descending serotonergic/adrenergic pain pathways, acted locally by reducing calcium flux in sensory neurons (like a CB1 antagonist), opened peripheral potassium channels and involved release of the endocannabinoid anandamide — demonstrating antinociception in neuropathic pain (a preclinical result).
Hemopressin acts on satiety and pain, not reward
Combining pharmacological-challenge MRI with c-Fos mapping in mice, systemic hemopressin activated the feeding-control nuclei of the mediobasal hypothalamus and the pain regions of the periaqueductal grey and dorsal raphe, but — unlike the synthetic CB1 inverse agonist AM251 — did NOT activate the brain's reward centres. This distinct 'satiety not reward' signature suggests hemopressin could curb appetite and pain without the psychiatric side effects of synthetic CB1 blockers (a preclinical result).
How hemopressin binds CB1
Circular dichroism, NMR and molecular docking of hemopressin and its active fragment hemopressin(1-6) showed that turn structures in the central part of the peptide are critical for an effective interaction with CB1. The binding analysis revealed similarities and differences versus the accepted CB1 pharmacophore, suggesting new chemical scaffolds for designing CB1 antagonist lead compounds (a structural study).
No Established Human Dose
Hemopressin is a hemoglobin-derived peptide that has never been given to people as a treatment. The work is in animals and cells, where hemopressin is given orally or by injection at experimental amounts that do not carry over to people. No regulator has approved any dose, and no published human dose exists, so no amount is printed here.
What this rests on: PMID 18077343, PMID 20505104, PMID 24703998.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Hemopressin (Hp) is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Hemopressin (Hp) has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Hemopressin (Hp), before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Hemopressin (Hp) stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Hemopressin (Hp). What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
How long it stays in the body: a half-life of not established for humans as a drug; a hemoglobin-derived peptide. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Hemopressin (Hp). Results reported in the studies are under Published Research.
Source: half-life: PMID 27748182.
Side effects, and when to stop or get help
From the Side Effects section: No human adverse-event data exist: no published study has administered hemopressin to people; In animals it reduces food intake without obvious side effects and, unlike synthetic CB1 blockers, appears to spare reward circuits (PMIDs 20505104, 23542442) — a preclinical signal, not a human safety profile; As a CB1 inverse agonist it is in the same pharmacological class as rimonabant, which was withdrawn for psychiatric side effects — a reason hemopressin's reward-sparing profile is studied carefully; Material sold online as 'hemopressin' is an unregulated research chemical of unverified content. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Hemopressin (Hp). Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Hemopressin is a research peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status”).
Interactions
Unknown: a PubMed search for human interaction studies of Hemopressin (Hp) (reviewed 2026-11-06) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Hemopressin (Hp) products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a drug: Drugs@FDA and the openFDA label endpoint hold no record, and FDA GSRS and ChEMBL hold no substance record for hemopressin (searched November 6, 2026)). Sport: Not on the 2026 List.
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
Hemopressin is a research peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status.
Contraindications & Cautions
Hemopressin has no approved use and no label. These points reflect its research status.
Legal Status
Hemopressin is a hemoglobin-derived peptide studied as a research compound; it is not a drug and is not approved in any country.
Frequently Asked Questions
?What is hemopressin?
A short peptide (nine amino acids; rat sequence PVNFKFLSH) cut from the alpha chain of hemoglobin. It was the first peptide found to bind the CB1 cannabinoid receptor, where it acts as an antagonist/inverse agonist.
?What does it do?
By switching CB1 off it reduces food intake — a lead against obesity (PMID 20505104) — and relieves inflammatory and neuropathic pain (PMIDs 18077343, 24703998), apparently acting on satiety and pain circuits without the reward effects of synthetic CB1 blockers (PMID 23542442).
?Is it the same as the endocannabinoids?
No. The endocannabinoids (anandamide, 2-AG) are fatty molecules that activate CB1; hemopressin is a peptide that blocks CB1. Its extended forms (RVD-/VD-hemopressin, the 'pepcans') act differently, and there is debate whether short hemopressin is endogenous or an extraction fragment of the longer peptide.
?Is it approved or available to buy?
No. Hemopressin is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as hemopressin is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [mechanism] Heimann AS, et al. "Hemopressin is an inverse agonist of CB1 cannabinoid receptors." Proc Natl Acad Sci U S A, 2007;104(51):20588-93. PMID: 18077343.
- [review] Macedonio G, et al. "Hemopressin Peptides as Modulators of the Endocannabinoid System and their Potential Applications as Therapeutic Tools." Protein Pept Lett, 2016;23(12):1045-1051. PMID: 27748182.
- [animal] Dodd GT, et al. "The peptide hemopressin acts through CB1 cannabinoid receptors to reduce food intake in rats and mice." J Neurosci, 2010;30(21):7369-76. PMID: 20505104.
- [animal] Toniolo EF, et al. "Hemopressin, an inverse agonist of cannabinoid receptors, inhibits neuropathic pain in rats." Peptides, 2014;56:125-31. PMID: 24703998.
- [animal] Dodd GT, et al. "Central functional response to the novel peptide cannabinoid, hemopressin." Neuropharmacology, 2013;71:27-36. PMID: 23542442.
- [mechanism] Scrima M, et al. "Binding of the hemopressin peptide to the cannabinoid CB1 receptor: structural insights." Biochemistry, 2010;49(49):10449-57. PMID: 21062041.
- [other] UniProt P69905 (HBA_HUMAN), read November 6, 2026: hemopressin is a short peptide derived by proteolytic cleavage from the alpha chain of hemoglobin (HBA1/HBA2 gene products); the originally described rat peptide is the nonapeptide Pro-Val-Asn-Phe-Lys-Phe-Leu-Ser-His (PVNFKFLSH). https://www.uniprot.org/uniprotkb/P69905/entry
- [other] Hemopressin was identified by screening endogenous brain peptides for ligands of the CB1 cannabinoid receptor, and its N-terminally extended forms (RVD- and VD-hemopressin, the 'pepcans') were later described; whether hemopressin is itself endogenous or an extraction fragment of the longer RVD-hemopressin is discussed in the endocannabinoid-modulator review carded on this page (read November 6, 2026).
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 6, 2026: no application and no label record for hemopressin. It is a hemoglobin-derived peptide, not a registered drug; FDA GSRS and ChEMBL hold no substance record for it.
Sources & Citations
The six studies carded above were read from their PubMed records on November 6, 2026. Identity comes from UniProt (P69905, hemoglobin alpha chain); hemopressin's origin as a hemoglobin fragment, its status as the first peptide CB1 ligand (inverse agonist), its appetite- and pain-reducing, reward-sparing actions, and the debate over its endogenous versus extraction origin are from the discovery paper, review and studies carded here; the absence of US approval and of a drug substance record from Drugs@FDA, openFDA, FDA GSRS and ChEMBL was checked the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.