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leucovorin + tegafur + uracil (leucovorin + UFT / UFT/leucovorin)

✓ Approved

Merck KGaA · TYMS · Small Molecule

What is leucovorin + tegafur + uracil?

leucovorin + tegafur + uracil is a small molecule developed by Merck KGaA. It is approved for therapeutic indications via injectable (others) or intravenous (iv) or oral (po).

Drug Profile

Brand Namesleucovorin + UFT, UFT/leucovorin
CompanyMerck KGaA
Drug ClassSmall Molecule
Molecular TargetTYMS
RouteInjectable (Others), Intravenous (IV), Oral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Merck KGaA

Mechanism of Action

Molecular Targets

leucovorin + tegafur + uracil acts on 1 molecular target:

TYMSthymidylate synthetase (DKCD, TMS)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

leucovorin + tegafur + uracil is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Colorectal cancer✓ Approved

Related Research Articles

PubMedAnalytical chemistry2026-11-11

Sequencing Deoxyuracil at Single-Base Resolution via a Hydrazine Reagent-Induced U-to-A Transition.

Xue Chen-Yu CY, Liu Ya-Hong YH, Cao Yu-Chao YC, Zhang Run-Hong RH et al.

Uracil is a canonical base in RNA, yet its presence in DNA represents the most common non-canonical modification, with broad implications for diverse physiological processes. However, due to the lack of suitable analytical methods, the distribution and biological functions of deoxyuracil (dU) in the genome remain largely unexplored. Herein, a single-base-resolution sequencing method for dU based on chemical labeling is established. By converting dU into abasic (AP) sites, we achieve specific chemical derivatization of the target residues via the aldehyde-hydrazine reaction. Two hydrazine reagents2-hydrazinyl-4,6-dimethoxy-1,3,5-triazine (MeO) and its methylamino analogue (MeNH)are introduced, both of which are base analogues rich in N or O. During subsequent PCR amplification with Vent (exo-) DNA polymerase, a base transition from uracil (sequenced as T) to adenine (A) is induced, serving as the readout for identifying target sites. Our method is simple, cost-effective, and easy to operate. Sample preparation requires only two enzymatic and labeling steps, and target gene analysis can be completed by Sanger sequencing. The practicality of this approach is validated in complex biological samples, providing an easy-to-use tool for investigating the hotspots of dU in the genome.

PMID 43010428
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PubMedZhonghua zhong liu za zhi [Chinese journal of oncology]2026-11-11

[Comparison of efficacy and safety between TAE combined with FOLFOX-HAIC or RALOX-HAIC in the treatment of hepatocellular carcinoma].

Zhang M M, Chang X J XJ, Gao X D XD, Kong H F HF et al.

Objective: To compare the efficacy and safety of hepatic arterial infusion chemotherapy (HAIC) using the FOLFOX regimen, consisting of oxaliplatin, leucovorin, and 5-fluorouracil, with those of HAIC using the RALOX regimen in patients with intermediate-advanced hepatocellular carcinoma. Methods: A total of 239 patients with primary hepatocellular carcinoma who received transarterial embolization (TAE) combined with FOLFOX-HAIC or RALOX-HAIC at the Fifth Medical Center of Chinese PLA General Hospital between January 2022 and October 2024 were retrospectively enrolled. Patients in the FOLFOX-HAIC and RALOX-HAIC groups were matched at a ratio of 2∶1 using propensity score matching (PSM), resulting in 103 patients in the FOLFOX-HAIC group and 68 patients in the RALOX-HAIC group. The objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), overall survival (OS), and adverse events were compared between the two groups. Results: After PSM, there were no statistically significant differences in baseline characteristics between the FOLFOX-HAIC and RALOX-HAIC groups, with all P values greater than 0.05. According to Response Evaluation Criteria in Solid Tumors version 1.1, the ORR was 37.9% (39/103) in the FOLFOX-HAIC group and 33.8% (23/68) in the RALOX-HAIC group, while the DCR was 84.5% (87/103) and 76.5% (52/68), respectively. No significant differences were observed between the two groups, with P values of 0.707 and 0.266, respectively. According to modified Response Evaluation Criteria in Solid Tumors, the ORR was 49.5% (51/103) in the FOLFOX-HAIC group and 45.6% (31/68) in the RALOX-HAIC group, while the DCR was 84.5% (87/103) and 76.5% (52/68), respectively. The differences were also not statistically significant, with P values of 0.729 and 0.266, respectively. The median PFS was 11.9 months in the FOLFOX-HAIC group and 10.0 months in the RALOX-HAIC group, while the median OS was 23.1 months and 17.2 months, respectively, with no statistically significant differences between the two groups, both P=0.400. The incidences of grade 1-2 adverse events were 62.1% and 66.2% in the FOLFOX-HAIC and RALOX-HAIC groups, respectively, while the incidences of grade 3-4 adverse events were 36.9% and 29.4%, respectively. No significant differences were observed between the two groups, with all P values greater than 0.05. The most common grade 3-4 adverse events in both groups were increased aspartate aminotransferase levels (29.1% and 19.1%), increased alanine aminotransferase levels (20.4% and 20.6%), and thrombocytopenia (16.5% and 25.0%). Conclusions: In patients with intermediate-advanced hepatocellular carcinoma receiving TAE combined with HAIC, FOLFOX-HAIC and RALOX-HAIC showed comparable efficacy and safety. RALOX-HAIC may serve as a potential alternative to FOLFOX-HAIC.

PMID 43010747
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PubMedChemical communications (Cambridge, England)2026-11-10

Formal [4+1] cyclization of skipped enynes with uracil-derived enaminones: metal-free access to spirocyclopentadienes.

Megavath Vinod V, Kumar Rituraj R, Yaragorla Srinivasarao S

Herein, we report a metal-free approach to construct spirocyclopentadienes via the formal (4C+1C) cyclization of uracil-derived push-pull enaminones and vinylpropargyl alcohols. The reaction is promoted by PTSA in hexafluoroisopropanol (HFIP) and proceeds via the dehydrative formation of 1,3-enynes, followed by a base-mediated annulation. This protocol provides a highly efficient and step-economical strategy to construct diverse spiropentadiene frameworks.

PMID 43007165
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PubMedAnnals of surgical oncology2026-11-10

Poor Imaging Response to FLOT is Associated with Worse Pathologic Features and Survival in Gastroesophageal Adenocarcinoma.

Park Jin-Soo JS, Allison Frances F, Allen Jonathan J, Jang Raymond R et al.

Little is known about the outcomes of patients with gastroesophageal adenocarcinoma (GEA) who respond poorly to neoadjuvant FLOT (5-fluorouracil, leucovorin, oxaliplatin, docetaxel) on imaging. We aimed to determine whether imaging non-response to FLOT was associated with worse pathologic features, recurrence patterns, and survival outcomes. Patients with GEA who received neoadjuvant FLOT from January 2017 to April 2025 were retrospectively analyzed. Staging and re-staging computed tomography and positron emission tomography were used to determine tumor response, stratifying the cohort into FLOT responders or non-responders (FNRs). Pathologic features, overall survival (OS) and event-free survival (EFS) were compared between the two groups. Survival data from 193 patients were analyzed: 116 (60.1%) were responders and 77 (39.9%) were FNR; 24 patients in the FNR group developed metastases and were not included in pathologic analysis (n = 169). FNRs had worse performance status, more advanced ypT and ypN stage, less pathologic tumor regression, and higher rates of lymphovascular and perineural invasion than responders. Imaging response to FLOT was significantly associated with pathologic tumor regression grade (p < 0.001). Median OS was lower in the FNR group (24.6 vs. 67 months, log rank p < 0.001), as was median EFS (13 vs. 32 months, log rank p < 0.001). FLOT non-response was a prognostic factor for OS (hazard ratio 1.989; 95% confidence interval 1.079-3.669; p = 0.028) on multivariable analysis. In the 81 patients who experienced recurrence after resection, there was no difference in OS and EFS with imaging response. Patients with GEA with poor response to FLOT on imaging demonstrated significantly worse pathologic features and OS and EFS.

PMID 43004099
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PubMedMicrobiology spectrum2026-11-09

A dual endogenous selectable marker system for Aspergillus flavus and its application in characterizing nsdD function in development and aflatoxin biosynthesis.

Zhao Xiu-Lan X-L, Zhang Qi Q, Li Pei-Wu P-W, Luo Chao-Xi C-X

Aspergillus flavus poses a significant threat to global food security and public health, as it not only triggers severe mold spoilage in staple crops like peanuts and corn but also produces aflatoxin, a potent carcinogen. However, genetic manipulation of this fungus is notoriously challenging due to its inherent insensitivity to conventional antibiotics. To overcome this barrier, we established a robust, fully endogenous genetic transformation system for a highly toxigenic wild-type strain, A. flavus-SD, using polyethylene glycol (PEG)-mediated protoplast transfection with two selectable markers: pyrG (uracil auxotrophy/5-FOA counterselection) and a β-tubulin E198A point mutation (carbendazim resistance). We successfully constructed the tool strains with a ΔpyrG mutation, which were used for gene knockout and overexpression, and the β-tubulin E198A mutant was used for gene complementation. To validate the operational efficacy of this platform, we performed knockout, complementation, and overexpression of the nsdD gene as a test case. This study provides a reliable technical foundation for elucidating the molecular mechanisms governing aflatoxin biosynthesis and pathogenicity, thereby facilitating the identification of novel targets for A. flavus control. This study established a novel genetic transformation system for a highly toxigenic wild-type strain, Aspergillus flavus-SD, utilizing fully endogenous selectable markers: pyrG (uracil auxotrophy/5-FOA counterselection) and a β-tubulin E198A point mutation (carbendazim resistance). This platform eliminates the need for heterologous antibiotic resistance cassettes, thereby reducing biosafety concerns while enabling iterative genome editing through marker recycling. Using this system, we demonstrated its efficacy by validating the expected phenotypic changes upon nsdD manipulation, revealing a previously unrecognized trade-off between sclerotia formation and aflatoxin biosynthesis. This work provides a valuable, compliance-friendly resource for the fungal research community and lays a foundation for identifying novel targets to disrupt fungal persistence and mycotoxin production in agricultural settings.

PMID 43001793
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PubMedNature communications2026-11-08

Author Correction: Programmable DNA pyrimidine base editing via engineered uracil-DNA glycosylase.

Yi Zongyi Z, Zhang Xiaoxue X, Wei Xiaoxu X, Li Jiayi J et al.

PMID 42995206
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