Hypocretin-1 · OX-A
Orexin A (also called Hypocretin-1) is a 33-amino-acid neuropeptide produced by lateral hypothalamic neurons. It is one of two endogenous orexin peptides (along with Orexin B / Hypocretin-2) that promote wakefulness, arousal, appetite, and energy expenditure via OX1R and OX2R receptors. Loss of orexin neurons causes narcolepsy with cataplexy in humans - the major clinical context for orexin pharmacology.
Starting dose. Per investigational protocol
Intranasal preferred for CNS access. Reconstitute with bac water; refrigerate. Disulfide-containing - keep cold and protect from oxidation.
Start here. Every protocol below is ordered lowest-first. Begin at the smallest effective dose, hold about a week to assess tolerance, and step up only if needed.
Orexin A binds both orexin receptors (OX1R and OX2R) in approximately equal affinity, distinguishing it from Orexin B which is OX2R-selective:
Selectively expressed on dopaminergic VTA neurons and locus coeruleus norepinephrine neurons - drives reward-related behavior and arousal.
Expressed on tuberomammillary nucleus histaminergic neurons - drives wake-promotion. OX2R signaling is the primary wake-promoting orexin pathway (basis of OX2R-selective insomnia therapy with the antagonist class).
Endogenous orexin neurons fire during wake state and silence during sleep. Loss of these neurons (autoimmune destruction in narcolepsy with cataplexy) produces the disease. Exogenous Orexin A can theoretically substitute - main delivery challenge is CNS penetration.
Lateral hypothalamic orexin signaling stimulates feeding behavior - high-dose orexin administration produces hyperphagia.
Orexin signaling increases sympathetic tone - heart rate, blood pressure, energy expenditure all rise. Relevant to cardiovascular caution at high doses.
Two intramolecular disulfide bonds - chemistry-incompatible with copper-conjugated peptides like GHK-Cu.
Acute wakefulness within 15-30 min of intranasal dose.
Effects fade with plasma clearance.
No long-term cumulative effects characterized.
Each reference below was re-fetched from its PubMed record, and the quoted sentence was confirmed to appear in that abstract and to support the claim it sits under. Follow any of them to read the source.
Orexin-A (OXA) is a neuropeptide with neuroprotective effect by reducing cerebral ischemia/reperfusion injury (CIRI).
Orexin-A (OXA) is a neuropeptide with neuroprotective effect by reducing cerebral ischemia/reperfusion injury (CIRI).
Evidence scope. Preclinical cerebral ischemia/reperfusion work; not intranasal or subcutaneous human dosing evidence.
Claims we could not support
No abstract we checked supports these for this molecule at this route. That is not the same as saying they are false — it marks where the evidence is missing.
Dose/route: Per investigational protocol via Intranasal (primary) or SubQ, Variable. No checked live PubMed abstract supported this complete molecule/formulation/route/dose/frequency combination.
Primary safety claim: Nasal irritation (intranasal). No checked live abstract directly established this as the primary concern for the card's exact formulation and regimen.
Plasma
Intranasal, longer SubQ
Wakefulness/arousal
Intranasal preferred for CNS access; subQ has BBB penetration challenge
Per dose
Hepatic/renal proteolysis
Storage. Refrigerate. Light-sensitive. Reconstituted: 14-21 days. Disulfide-containing - keep cold.
Not FDA-approved. Investigational status only. WADA: not specifically prohibited but may fall under stimulant regulations in sport contexts.
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