AC-SDKP (TB-500 Fragment) half-life & pharmacokinetics

Reported half-life

Short; plasma half-life in rodents is approximately 5–10 minutes following intravenous bolus, primarily due to rapid hydrolysis by angiotensin-converting enzyme (ACE). ACE-inhibitor co-administration dramatically extends apparent exposure.

The half-life and pharmacokinetic profile of AC-SDKP (TB-500 Fragment) reported above is drawn from the published pre-clinical literature. Plasma half-life describes the time taken for the circulating concentration to fall by half after a single dose; tissue half-life — which may be longer for peptides retained in specific organs or matrices — is a distinct and often more relevant parameter for healing research, where the duration of exposure at the injury site matters more than the systemic exposure profile.

Routes of administration studied

• Subcutaneous injection
• Intravenous infusion (research models)

Different routes produce materially different pharmacokinetic profiles for the same peptide. Subcutaneous administration generally produces flatter, more sustained plasma profiles than intravenous bolus dosing; intraperitoneal administration (common in rodent models) is not directly translatable to human routes; oral administration faces the additional challenge of luminal and brush-border peptidase degradation, which is why most research peptides have very low oral bioavailability without protective formulation.

Drug class

Endogenous tetrapeptide; haematopoietic regulator and anti-fibrotic agent

Mechanism context

Half-life interpretation depends on the underlying mechanism. AC-SDKP (TB-500 Fragment) acts as follows:

AC-SDKP (N-acetyl-Ser-Asp-Lys-Pro) is a constitutively released tetrapeptide generated from the N-terminus of thymosin beta-4 through sequential cleavage by prolyl oligopeptidase. Its primary catabolic route is hydrolysis at the Pro–Gly bond by angiotensin-converting enzyme (ACE, somatic form). This biochemical relationship is clinically relevant: ACE inhibitors, by blocking AC-SDKP degradation, raise endogenous plasma AC-SDKP concentrations by approximately four- to five-fold in humans, a phenomenon documented by Rousseau and colleagues (Am J Hypertension, 1995). This rise in endogenous AC-SDKP is one proposed mechanism underpinning the anti-fibrotic benefits of ACE-inhibitor therapy in cardiovascular and renal disease, beyond the peptide's haemodynamic effects.

See the full AC-SDKP (TB-500 Fragment) research profile for the complete mechanism summary, history, study citations, and references.

Practical considerations

Short plasma half-life does not necessarily mean short duration of biological effect. Many peptides — including BPC-157, GHK-Cu, and the thymosin-derived compounds — exhibit tissue retention or mechanistic effects (gene expression, signalling cascades) that outlast plasma exposure by hours to days. The pharmacological half-life and the biological-effect half-life are distinct parameters that must both be specified in any rigorous research design. Repeated-dose protocols should account for accumulation only where tissue half-life is genuinely long; for most peptides with short plasma half-life and rapid degradation, accumulation is not a practical concern.

For dose ranges in published research, see the dosing reference page. For reconstitution guidance, see the reconstitution reference page.