Independent · non-commercial · publishes on a quarterly cycle|Current cycle 2026 Q3
Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

Glutathione — pharmacology

Molecular targets, mechanism of action, pharmacokinetics and interactions as characterised in humans.

Document identifier
CEI-MN-046/2
Series
Compound monograph
Version
1.3
Published
06 May 2026
Last reviewed
06 May 2026
Next review
06 May 2028
Identifier
10.71829/cei.mono.46
Certainty
Low
Cycle
2026 Q2

§2Pharmacology

§2.1Molecular targets

Table 2. Molecular targets recorded for Glutathione, with the character of the interaction and the potency where the Institute holds it.

TargetInteractionNote
Glutathione peroxidases and S-transferasesSubstrate and cofactorThe principal intracellular thiol antioxidant and phase II conjugation cofactor
Reactive electrophilesDirect conjugationNon-enzymatic and enzymatic conjugation of electrophilic species

§2.2Mechanism of action

Glutathione is the dominant intracellular low-molecular-weight thiol and the cofactor of the glutathione peroxidase and S-transferase systems. Administered glutathione is largely degraded extracellularly by gamma-glutamyl transpeptidase to its constituent amino acids, which are then taken up and used for intracellular resynthesis; the Institute notes that this makes cysteine availability, rather than glutathione administration, the rate-limiting consideration, and is the pharmacological rationale for N-acetylcysteine as an alternative.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈10 min after intravenous administration
Time to maximum concentration
immediate on infusion
Volume of distribution
largely extracellular when administered
Plasma protein binding
not extensively bound
Clearance
rapid, largely renal and via gamma-glutamyl transpeptidase
Bioavailability
oral bioavailability of intact glutathione is low and contested

Extracellular hydrolysis by gamma-glutamyl transpeptidase and dipeptidases, with renal excretion. Intracellular concentrations are governed by de-novo synthesis, not by administered glutathione.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.60.801122Time after first dose (hours)Relative concentrationt max ≈ 0 ht½ ≈ 1 h
Modelled profileSimulated observationsDose administration
Figure 2. Illustrative. Plasma concentration–time profile reconstructed by the Institute from the published half-life and time-to-maximum-concentration parameters using a one-compartment model with first-order absorption. The curve is not digitised from a published figure and its vertical scale is relative. It is published to convey the shape of the profile and the approach to steady state, not to supply a concentration at any time point.

§2.4Interactions

  • Cisplatin and other electrophilic chemotherapeutics — glutathione conjugation may reduce efficacy

References cited on this page

References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.

  1. D’Hondt M, Bracke N, Taevernier L, Gevaert B, Verbeke F, Wynendaele E, De Spiegeleer B. Related impurities in peptide medicines. Journal of Pharmaceutical and Biomedical Analysis 2014;101:2–30. doi:10.1016/j.jpba.2014.06.012 · PMID 25044089
  2. Manning MC, Chou DK, Murphy BM, Payne RW, Katayama DS. Stability of protein pharmaceuticals: an update. Pharmaceutical Research 2010;27(4):544–575. doi:10.1007/s11095-009-0045-6 · PMID 20143256

Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.

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