Thymidine

-0.93

-0.93

73.5 mg/mL

Water 50 (mg/mL)

Solid; [Merck Index] White odorless powder; [Alfa Aesar MSDS]

Solid

161 Ų [M+Na]+ [CCS Type: DT; Method: single field calibrated with Agilent tune mix (Agilent)]；151.22 Ų [M-H]- [CCS Type: DT; Method: single field calibrated with Agilent tune mix (Agilent)]

164.51 Ų [M+Na]+ [CCS Type: DT; Method: stepped-field]；157.04 Ų [M-H]- [CCS Type: DT; Method: stepped-field]

161.6 Ų [M+Na]+ [CCS Type: DT; Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]；154.1 Ų [M-H]- [CCS Type: DT; Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]

154.2 Ų [M-H]-；161.2 Ų [M+Na]+

This chemical does not meet GHS hazard criteria for 97.6% (121 of 124) of all reports.

Not Classified；Reported as not meeting GHS hazard criteria by 121 of 124 companies (only 2.4% companies provided GHS information). For more detailed information, please visit ECHA C&L website.

Aggregated GHS information provided per 124 reports by companies from 4 notifications to the ECHA C&L Inventory.；Reported as not meeting GHS hazard criteria per 121 of 124 reports by companies.；There are 3 notifications provided by 3 of 124 reports by companies with hazard statement code(s).；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Chemical: Thymidine

Status: Active Update: 02-09-2014 https://echa.europa.eu/registration-dossier/-/registered-dossier/15994

Thymidine: Does not have an individual approval but may be used under an appropriate group standard

Chemical: Thymidine

Status: Active Update: 02-09-2014 https://echa.europa.eu/registration-dossier/-/registered-dossier/15994

Thymidine: Does not have an individual approval but may be used under an appropriate group standard

Thymidine acts systemically as a biochemical modulator to optimize the efficacy and reduce the toxicity of standard anti-metabolite chemotherapeutic agents. Its core action is the metabolic modulation of key enzymes in the DNA salvage pathway, which results in the potentiation of anti-tumor effects (e.g., when combined with 5-Fluorouracil) or protection against host toxicity (e.g., host cell rescue from Methotrexate toxicity). Furthermore, TdR, through its conversion to dTTP, significantly accelerates DNA replication fork progression and helps alleviate replication stress in rapidly proliferating cells, a fundamental effect that contributes to its role in preserving genomic stability and altering the selectivity of drug therapy.

The primary molecular function of Thymidine is its role as a precursor in the DNA salvage pathway, which it exploits to act as a potent biochemical modulator of anti-metabolite chemotherapy. Unlike its use as a traditional drug, thymidine's effect is achieved by manipulating the intracellular balance of deoxyribonucleotide triphosphate (dNTP) pools, which are essential for DNA synthesis and repair. Upon administration, thymidine is rapidly salvaged and phosphorylated by thymidine kinases to form dTTP (deoxythymidine triphosphate). This supplementation significantly increases the intracellular concentration of both dTTP and dGTP pools. This alteration of dNTP balance is directly responsible for thymidine's observed therapeutic effects, which are dependent on the co-administered drug. The elevated dTTP pools influence the metabolism of cytotoxic drugs. For example, it is thought to enhance the activation and incorporation of the active cytotoxic form of 5-Fluorouracil (FU) into DNA and RNA. The increase in dTTP and dGTP is linked to the observed acceleration of DNA replication fork progression in various cell types.

Thymidine is primarily degraded (catabolized) by thymidine phosphorylase to the nucleobases and the 2-deoxy-α-D-ribose 1-phosphate moiety. Thymine, the pyrimidine nucleobase of doxribtimine, is subsequently catabolized to dihydrothymine and ultimately to γ-amino-isobutyric acid and CO2.

The absolute bioavailability of thymidine following oral administration has not been determined. The median time to peak plasma concentration (Tmax) was approximately four hours.

Urinary excretion of intact thymidine was <1% of the dose in healthy subjects following an oral administration.

Thymidine's transfer across the blood-brain barrier is generally considered extremely low, with studies suggesting an active transport system in the choroid plexus transfers it into the cerebrospinal fluid (CSF) before it enters brain cells.