LOG 04 / DOSE-RESPONSE / 25 nmol/kg
DSIP dosage, as logged in the research record
The doses, routes, and half-life that appear in published studies, recorded as study parameters, never as a protocol or recommendation.
The short version
This page logs the DSIP dosage figures that appear in published studies. It is a record of what researchers gave to animals and to small groups of patients, not a guide for use and not a protocol. The number that comes up most in human studies is 25 nmol/kg given by vein [2]. Animal studies used very different amounts depending on the species and the question, from fractions of a microgram in the rat brain to about 100 micrograms per kilogram in mice [5]. One quirk matters a lot: DSIP breaks down in the blood within minutes, so its half-life is extremely short. Another quirk is that more is not reliably better, the dose-response is U-shaped, so middle doses can outperform high ones. No approved dose exists for any use, and nothing here should be read as a dosing instruction.
DSIP dosage in human studies
Across the human research record, the most frequently used DSIP dosage was 25 nmol/kg of body weight, given intravenously [2]. That figure recurs in the insomnia work, where 25 nmol/kg improved disturbed sleep with effects emerging in the second hour after injection [2], and in the neuroendocrine work, where the same 25 nmol/kg intravenous dose reduced plasma ACTH-like immunoreactivity for at least three hours without changing cortisol [4]. Other human studies used multi-injection courses, for example a 10-injection clinical course reported to normalize sleep in six of seven patients [9], without specifying a per-dose amount in the abstract. These are study parameters, recorded for documentation. They are not titration schedules, they are not adjusted for any individual, and they do not constitute a recommended dose, because DSIP is not an approved drug and has no validated human dosing standard.
DSIP peptide dosage in animal models
Animal DSIP peptide dosage spans a wide range because the species and endpoints differ. In rat growth-hormone studies, in-vivo intracerebroventricular doses of 0.1-10 micrograms were used, with a minimal effective dose around 0.1 microgram. Rat neuroprotection work used 120 micrograms/kg intranasally, and rat anticonvulsant studies used 0.1-1 mg/kg, most effective at 1 mg/kg. In cats, sleep studies used 120 nmol/kg subcutaneously. The mouse longevity work with the Deltaran preparation used roughly 100 micrograms/kg (2.5 micrograms per mouse) subcutaneously, given five consecutive days per month [5]. The 2024 fusion-peptide study administered 100 nM in saline for five consecutive days in a mouse insomnia model [6]. These figures are not interchangeable with human exposure, and the cross-species differences are part of why DSIP's effects have been so hard to translate.
Half-life, stability, and the dsip peptide nasal spray question
DSIP has a very short circulating half-life. An enzyme-immunoassay clearance study in dogs, monkeys, and rats reported plasma half-lives on the order of only a few minutes, attributed to rapid degradation by aminopeptidases and plasma proteins, and there is no validated human pharmacokinetic profile. That instability shapes how DSIP appears in research: it is a short peptide subject to rapid enzymatic breakdown, which is why the naturally phosphorylated analog DSIP-P and other synthetic analogs are reported as more stable or potent in some assays. On the question of a dsip peptide nasal spray: the published routes studied are intravenous (human and animal), intracerebroventricular (rodent), subcutaneous (cat, mouse), intranasal (in a rat neuroprotection study), and in-vitro perifusion. Intranasal DSIP appears in the animal literature, but there is no approved, standardized nasal-spray product and no human nasal-route efficacy or pharmacokinetic data, so any nasal formulation sold commercially is an unstandardized research preparation, not a validated delivery system.
The parabolic dose-response
One feature makes DSIP dosage genuinely hard to interpret: a reported parabolic, or U-shaped, dose-response, in which the effect rises and then falls as the dose increases, so intermediate doses can be more effective than high ones. This non-monotonic pattern means that scaling a dose up offers no guarantee of a stronger effect and may produce a weaker one, which undercuts any simple more-is-better reasoning. Combined with the minutes-long half-life and the absence of a validated human pharmacokinetic profile, the parabolic curve is a major reason the DSIP literature has never converged on a standard effective dose. It is also a reason the community reports on this compound vary so widely: without a reliable dose-response relationship, two people using similar amounts can have very different experiences, a pattern visible across the reported effects.