Ac-SDKP vs DSIP

Inhibits hematopoietic stem cell entry into S-phase. Blocks TGF-β1-mediated fibroblast activation, reducing collagen deposition. Promotes angiogenesis via VEGF upregulation. Regulated in vivo by ACE enzyme.

Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is an endogenous tetrapeptide generated from the N-terminus of thymosin beta-4 by the enzyme prolyl oligopeptidase, with further regulation by angiotensin-converting enzyme (ACE), and is characterized by roles in hematopoietic progenitor regulation and anti-fibrotic signaling in renal, cardiac, and vascular tissue. Ac-SDKP inhibits collagen synthesis and fibroblast proliferation, reduces TGF-beta-1-mediated fibrotic signaling, and promotes anti-inflammatory macrophage polarization in preclinical models, suggesting a role in tissue homeostasis downstream of the thymosin beta-4 pathway. Preclinical studies in rodent models of renal fibrosis and systemic lupus erythematosus — predominantly from the NIH-funded Rhaleb and Carretero laboratory at Henry Ford Health — have demonstrated that exogenous Ac-SDKP reduces collagen deposition and inflammatory infiltrate; no human clinical trials have been completed or indexed in PubMed. Ac-SDKP has no FDA approval and no approved indication in any jurisdiction; it is studied as a research compound with a plausible anti-fibrotic mechanism and consistent preclinical evidence, but extrapolation of rodent findings to human therapeutic outcomes has not been validated by any clinical investigation.

Neuropeptide that modulates sleep architecture by promoting delta-wave sleep patterns. Reduces stress hormones including ACTH and cortisol, and interacts with hypothalamic-pituitary pathways to support recovery and circadian regulation.

DSIP (delta sleep-inducing peptide) is a nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) originally isolated from the cerebral venous blood of sleeping rabbits by Schoenenberger and Monnier in 1977, subsequently investigated for roles in sleep regulation, stress response modulation, and neuroendocrine activity across multiple neuropeptide systems. DSIP is proposed to act through modulation of GABAergic and serotonergic neurotransmission and to influence the release of multiple pituitary hormones including LH, GH, and ACTH, though no definitive receptor has been identified and its endogenous physiological role in mammalian sleep architecture remains incompletely understood. Foundational rodent studies demonstrated sleep-promoting effects following central or peripheral administration, and early small human EEG studies reported possible effects on sleep architecture; results have been inconsistent across studies, independent replication has been poor, and sleep-inducing activity in humans has not been established by any controlled clinical trial. DSIP has no FDA approval and no approved therapeutic indication in any jurisdiction; it is a research compound with an unconfirmed receptor target, an unclear mechanism of action, and an inconsistent human evidence base, and commercial availability through research peptide suppliers should not be interpreted as evidence of established clinical utility. DSIP dosage: No human clinical trial has established a reference dosing protocol for synthetic DSIP. Early human studies from the 1970s–80s used intravenous infusion at doses in the nanogram-to-microgram per kilogram range; these studies are dated and not replicated by modern clinical research standards. Research interest in DSIP has explored subcutaneous injection in research contexts. DSIP is a research compound with no approved human dosing guidelines for any indication.