D-Ribose-L-cysteine

D-Ribose-L-cysteine
Clinical data
Trade namesRiboCeine
Other namesRibCys; Ribose-cysteine
Identifiers
  • (4R)-2-[(1R,2R,3R)-1,2,3,4-Tetrahydroxybutyl]-1,3-thiazolidine-4-carboxylic acid
CAS Number
PubChem CID
ChemSpider
UNII
ChEBI
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC8H15NO6S
Molar mass253.27 g·mol−1
3D model (JSmol)
  • C1[C@H](NC(S1)[C@@H]([C@@H]([C@@H](CO)O)O)O)C(=O)O
  • InChI=1S/C8H15NO6S/c10-1-4(11)5(12)6(13)7-9-3(2-16-7)8(14)15/h3-7,9-13H,1-2H2,(H,14,15)/t3-,4+,5+,6+,7?/m0/s1
  • Key:AGZXTDUDXXPCMJ-HZYAIORGSA-N

D-Ribose-L-cysteine (RiboCeine) is a chemical compound developed as a cysteine prodrug intended to increase endogenous production of glutathione, a naturally occurring intracellular antioxidant. Structurally, it consists of D-ribose, a pentose sugar involved in cellular energy metabolism, chemically bound to L-cysteine, an amino acid required for glutathione biosynthesis.[1][2]

Background

Glutathione plays a central role in cellular redox balance, detoxification, and immune regulation. Its synthesis depends on the availability of several amino acid substrates, of which cysteine is typically the rate-limiting precursor under physiological conditions.[3]

Free L-cysteine is chemically unstable and readily oxidized in the gastrointestinal tract, which can limit its effectiveness when administered directly as a supplement. For this reason, a variety of cysteine-delivery strategies have been explored, including N-acetylcysteine (NAC) and other cysteine prodrugs.[4]

D-Ribose-L-cysteine was developed as an alternative cysteine-delivery compound intended to improve cysteine stability and intracellular availability for glutathione synthesis.[5]

Development and patents

D-Ribose-L-cysteine was developed by Herbert T. Nagasawa, a medicinal chemist formerly affiliated with the United States Department of Veterans Affairs and the University of Minnesota, whose research focused on sulfur amino acid metabolism and hepatic toxicology.[6]

The compound and its use as a glutathione-enhancing agent are protected by multiple patents, including United States Patent US 9,173,917 B2, assigned to Max International and the U.S. Department of Veterans Affairs.[7]

D-Ribose-L-cysteine has since been incorporated into dietary supplement formulations marketed by Max International, Inc. and LiveMax, LLC.[8]

Preclinical research

Animal studies

Multiple animal studies have investigated the biological activity of D-ribose-L-cysteine in models of oxidative stress and metabolic injury. These studies have reported that D-ribose-L-cysteine supplementation increases intracellular and tissue glutathione levels, improves antioxidant enzyme activity, and reduces markers of oxidative damage in rodents.[9][10][11]

In several experimental models, D-ribose-L-cysteine demonstrated equal or greater glutathione-enhancing effects compared with N-acetylcysteine, though these findings are limited to preclinical settings.[12]

In vitro studies

Cell culture studies have reported that D-ribose-L-cysteine increases glutathione levels and modulates oxidative stress responses in normal cell lines exposed to cytotoxic agents.[13]

Human research

As of 2025, only limited human clinical data on D-ribose-L-cysteine have been published.

A small randomized, placebo-controlled pilot trial conducted in 2023 evaluated the effect of a D-ribose-L-cysteine-containing supplement on serum glutathione levels in healthy adults over a 28-day period. According to results released by the study sponsor, participants receiving D-ribose-L-cysteine experienced a statistically significant increase in serum glutathione relative to baseline, with larger increases observed in older participants.[14]

The trial has not yet been independently replicated, and full peer-reviewed publication of the data has not been confirmed. Accordingly, the clinical significance of these findings remains preliminary.

Mechanism of action

D-Ribose-L-cysteine functions as a cysteine prodrug, delivering cysteine in a chemically protected form that may resist premature oxidation. After cellular uptake, enzymatic cleavage releases free L-cysteine, which can then enter the γ-glutamyl cycle for glutathione synthesis.[15]

This mechanism differs from N-acetylcysteine, which relies on de-acetylation and exhibits different absorption and metabolic characteristics. While both compounds ultimately increase cysteine availability, direct comparative data in humans remain limited.[16]

Regulatory status

D-Ribose-L-cysteine is regulated in the United States as a dietary supplement ingredient, not as a pharmaceutical drug. Products containing D-ribose-L-cysteine are subject to dietary supplement regulations under the Dietary Supplement Health and Education Act of 1994 (DSHEA), which prohibit claims that a product can diagnose, treat, cure, or prevent disease.[17]

No pharmaceutical drug approvals or therapeutic indications have been granted for D-ribose-L-cysteine by the U.S. Food and Drug Administration.[18]

Commercial use

D-Ribose-L-cysteine is used as an ingredient in several commercially marketed dietary supplements, particularly products promoted for general antioxidant support and cellular health. The primary commercial producers and distributors include Max International, Inc. and LiveMax, LLC.[19]

Reception and scientific commentary

Proponents of D-ribose-L-cysteine reference its patented chemical structure and the results of laboratory and animal investigations demonstrating increased glutathione production under experimental conditions.

However, independent medical experts generally emphasize that evidence of clinical benefit in humans remains insufficient, noting the absence of large-scale randomized trials or systematic reviews establishing long-term health outcomes of glutathione-related supplementation in healthy populations.[20][21]

References

  1. ^ Roberts JC, Charyulu RL, Zera RT, Nagasawa HT (April 1992). "Protection against acetaminophen hepatotoxicity by ribose-cysteine (RibCys)". Pharmacology & Toxicology. 70 (4): 281–285. doi:10.1111/j.1600-0773.1992.tb00472.x. PMID 1608914.
  2. ^ Kader T, Porteous CM, Williams MJ, Gieseg SP, McCormick SP (December 2014). "Ribose-cysteine increases glutathione-based antioxidant status and reduces LDL in human lipoprotein(a) mice". Atherosclerosis. 237 (2): 725–733. doi:10.1016/j.atherosclerosis.2014.10.101. PMID 25463112.
  3. ^ Ghezzi P (January 2011). "Role of glutathione in immunity and inflammation in the lung". International Journal of General Medicine. 4: 105–113. doi:10.2147/IJGM.S15618. PMC 3048347. PMID 21403800.
  4. ^ Maygarden SJ (1998). "The role of fine-needle aspiration cytology and core biopsy in the diagnosis of proliferative and atypical breast lesions". Anatomic Pathology. 2 (2): 165–196. PMID 9575375.
  5. ^ Roberts JC, Charyulu RL, Zera RT, Nagasawa HT (April 1992). "Protection against acetaminophen hepatotoxicity by ribose-cysteine (RibCys)". Pharmacology & Toxicology. 70 (4): 281–285. doi:10.1111/j.1600-0773.1992.tb00472.x. PMID 1608914.
  6. ^ From Digitalis to Ziagen: The University of Minnesota's Department of Medicinal Chemistry at 100 Years (PDF). University of Minnesota. 2013. Retrieved 2025-03-09.
  7. ^ US patent 9173917, Nagasawa HT, Cohen JF, "Methods for reducing oxidative stress in a cell with a sulfhydryl protected glutathione prodrug", issued 11 November 2015, assigned to Max International LLC and US Department of Veterans Affairs 
  8. ^ "Dietary Supplement Label Database (DSLD)". NIH Office of Dietary Supplements. Retrieved 2025-03-09.
  9. ^ Kader T, Porteous CM, Williams MJ, Gieseg SP, McCormick SP (December 2014). "Ribose-cysteine increases glutathione-based antioxidant status and reduces LDL in human lipoprotein(a) mice". Atherosclerosis. 237 (2): 725–733. doi:10.1016/j.atherosclerosis.2014.10.101. PMID 25463112.
  10. ^ Oz HS, Chen TS, Nagasawa H (August 2007). "Comparative efficacies of 2 cysteine prodrugs and a glutathione delivery agent in a colitis model". Translational Research. 150 (2): 122–129. doi:10.1016/j.trsl.2006.12.010. PMC 1991291. PMID 17656332.
  11. ^ Saltman AE (July 2015). "D-ribose-L-cysteine supplementation enhances wound healing in a rodent model". American Journal of Surgery. 210 (1): 153–158. doi:10.1016/j.amjsurg.2014.11.014. PMID 25935230.
  12. ^ Oz HS, Chen TS, Nagasawa H (August 2007). "Comparative efficacies of 2 cysteine prodrugs and a glutathione delivery agent in a colitis model". Translational Research. 150 (2): 122–129. doi:10.1016/j.trsl.2006.12.010. PMC 1991291. PMID 17656332.
  13. ^ Philips TJ, N'guessan BB, Dotse E, Abankwah JK, Appiah-Opong R (September 2025). "Riboceine and N-acetylcysteine protect normal prostate cells from chemotherapy-induced oxidative stress while selectively modulating the cytotoxicity of methotrexate and docetaxel in prostate (PC-3) and breast cancer (MCF-7) cells". Biomedicine & Pharmacotherapy. 190 118355. doi:10.1016/j.biopha.2025.118355. PMID 40690881.
  14. ^ "PRUVN reveals human clinical trial results of Max International's RiboCeine supplementation's impact on serum glutathione levels". PR Newswire. 2024-04-16. Retrieved 2025-03-09.
  15. ^ Roberts JC, Charyulu RL, Zera RT, Nagasawa HT (April 1992). "Protection against acetaminophen hepatotoxicity by ribose-cysteine (RibCys)". Pharmacology & Toxicology. 70 (4): 281–285. doi:10.1111/j.1600-0773.1992.tb00472.x. PMID 1608914.
  16. ^ Kelly G (1998). "Clinical applications of N-acetylcysteine" (PDF). Alternative Medicine Review. 3 (2): 114–127. PMID 9577247.
  17. ^ "Dietary Supplement Health and Education Act of 1994 (DSHEA)". U.S. Food and Drug Administration. Retrieved 2025-03-09.
  18. ^ "Drugs@FDA: FDA-Approved Drugs". U.S. Food and Drug Administration. Retrieved 2025-03-09.
  19. ^ "Dietary Supplement Label Database (DSLD)". NIH Office of Dietary Supplements. Retrieved 2025-03-09.
  20. ^ Ghezzi P (January 2011). "Role of glutathione in immunity and inflammation in the lung". International Journal of General Medicine. 4: 105–113. doi:10.2147/IJGM.S15618. PMC 3048347. PMID 21403800.
  21. ^ Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C (March 2012). "Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases". The Cochrane Database of Systematic Reviews. 2012 (3) CD007176. doi:10.1002/14651858.CD007176.pub2. PMC 8407395. PMID 22419320.
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