Drug Database
FL

fluorouracil (Carac, microsponge)

✓ Approved

Heron Therapeutics, Inc. · TYMS · Small Molecule

What is fluorouracil?

fluorouracil is a small molecule developed by Heron Therapeutics, Inc.. It is approved for therapeutic indications via transdermal.

Drug Profile

Brand NamesCarac, microsponge
CompanyHeron Therapeutics, Inc.
Drug ClassSmall Molecule
Molecular TargetTYMS
RouteTransdermal
StatusApproved
Sources: ClinicalTrials.gov, Heron Therapeutics, Inc.

Mechanism of Action

Molecular Targets

fluorouracil 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

fluorouracil is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersActinic keratosis✓ Approved

Related Research Articles

PubMedFrontiers in pharmacology2026-11-11

Mechanism-driven nano-therapeutic platform integrating plant-derived compounds and membrane-active peptides reprograms inflammatory, cell cycle arrest, cGAS-STING, and apoptotic gene expression to quench colorectal cancer.

Ibrahim Doaa D, Khater Safaa I SI, Abdelfattah-Hassan Ahmed A, Babteen Nouf A NA et al.

Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide, and its first-line chemotherapeutic, 5-fluorouracil (5-FU), is constrained by poor tumor selectivity, dose-limiting systemic toxicity, and the frequent emergence of drug resistance. Nanocarrier-based co-delivery of naturally derived, multi-targeted agents offers a promising strategy to enhance efficacy while limiting off-target harm. This study evaluated the antitumor effects of nanoformulated liposomal melittin peptides (LIP-MLT) and niosomal chrysin (NsCR), administered as monotherapy or as combined therapy (LIP-MLT/NsCR), against DMH-induced CRC in a rat model. CRC was induced by subcutaneous injection of DMH (1,2-dimethylhydrazine, 40 mg/kg, twice weekly) for 8 weeks. Sprague-Dawley rats (n = 120) were randomly divided into six groups: healthy control (CON); untreated colorectal tumour (CR-TUM); and DMH-induced rats treated with 5-fluorouracil (CR-TUM + FU5), liposomal melittin (CR-TUM + LIP-MLT), niosomal chrysin (CR-TUM + NsCR), or the combination (CR-TUM + LIP-MLT/NsCR). Oxidant/antioxidant status, inflammatory cytokines, and the transcriptional profiles of inflammatory, cell-cycle-arrest, apoptotic/antiapoptotic, cGAS-STING innate-sensing, mTOR, and angiogenesis/metastasis genes were assessed, together with histopathological and immunohistochemical evaluation. The untreated CR-TUM group showed pronounced tumor-markers elevation, anemia, oxidative damage, and a strong pro-inflammatory, immunosuppressive shift. Relative to CR-TUM, LIP-MLT/NsCR lowered the tumor markers CEA (3.1-fold), CA19-9 (3.5-fold), and CCSA (2.1-fold), and reduced the oxidative markers ROS (2.2-fold), MDA (1.8-fold), and NO (2.2-fold) while raising the antioxidants. It also decreased the pro-inflammatory mediators NF-κB (2.3-fold), IL-1β (2.4-fold), and TNF-α (1.7-fold) versus CR-TUM, reversing approximately 71% of the DMH-induced inflammatory signature. At the transcriptional level, the combination produced the strongest upregulation of the pro-apoptotic genes (Caspase-3, Caspase-8, BAX, and p53) with concurrent downregulation of the antiapoptotic mediators (Bcl-2, c-FLIP, and Survivin), and marked proliferative and metastatic drivers suppression, including CDK4, CDK6, cyclin D1, β-catenin, mTOR, MMP-9, and VEGF, alongside restoration of the CDK inhibitors p21, p27, and KLF4 and normalization of cGAS, STING, and IRF3 mRNA levels. LIP-MLT/NsCR further best-preserved body weight and colon length, lowered diarrhea and rectal-bleeding scores, restored colonic histopathological architecture, and most strongly diminished the immunoexpression of MMP-9 and VEGF relative to untreated cancer tissues. Taken together, the combined LIP-MLT/NsCR nanoformulation attenuated DMH-induced CRC progression to a greater extent than either monotherapy or conventional 5-FU, supporting the combined melittin-chrysin nanoformulation as a promising, multi-targeted strategy against colorectal cancer.

PMID 43011118
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PubMedOphthalmic epidemiology2026-11-11

Do Adjunctive Anti-scarring Agents Including Mitomycin-C Improve Glaucoma Tube Shunt Surgery: Systematic Review and Meta-analysis.

Tan Varen Zhi Zheng VZZ, Chee Miao Li ML, Lau Nicole Xer Min NXM, Yap Jayden Wen JW et al.

Adjunctive anti-scarring agents (ASAs), including mitomycin C (MMC), 5-Fluorouracil (5FU), corticosteroids and vascular endothelial growth factor antagonists (anti-VEGF), aim to improve glaucoma tube shunt (GTS) surgery by attenuating peri-endplate fibrosis. While used in trabeculectomy, ASAs are less established in GTS surgery, leading to varied practices. This systematic review and meta-analysis evaluated their efficacy and safety. Prospectively registered in PROSPERO (CRD 4,202,236,526), MEDLINE, EMBASE, and CENTRAL were searched for randomised controlled trials (RCTs) and comparative cohort studies (CCSs) comparing ASA and non-ASA use in GTS surgery. Outcomes included changes in intra-ocular pressure (IOP), anti-glaucoma medications, re-operation, and complication rates between baseline and post-operative months 3, 6, and 12. 28 studies (n = 1621 eyes) were included: 12 RCTs (n = 624 eyes) and 16 CCSs (n = 997 eyes). ASAs included MMC (n = 11/28), corticosteroids (n = 7/28), Anti-VEGF (n = 6/28), and 5FU (n = 2/28). Two studies used dual agents. ASA did not affect post-operative IOP [pooled difference (PD) 1.99 mmHg, 1.06 mmHg, 1.15 mmHg at month 3 (p = 0.059), 6 (p = 0.30), and 12 (p = 0.23), respectively]. ASA and MMC use resulted in fewer anti-glaucoma eyedrops required at month 3, 6, and 12 (PD = 0.56, 0.42, 0.49; p < 0.001, = 0.031, 0.013); (PD = 0.76, 0.73, 0.73; p < 0.001, = 0.001, < 0.013), respectively. Both increased hypotony development risk (OR = 2.06, p = 0.001; OR = 2.27, p = 0.001). All other complication rates were similar (all p > 0.05). The re‑operative rate was lower with MMC (OR = 0.42, p = 0.007). ASAs, particularly MMC, reduced glaucoma medication burden at 12 months, but increased the risk of post-operative hypotony.

PMID 43012868
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PubMedCombinatorial chemistry & high throughput screening2026-11-11

Exploring the Mechanism of Shenling Baizhu San in Mitigating Chemotherapy-Induced Intestinal Mucositis Based on Network Pharmacology and Multi-Omics Analysis.

Wang Sihan S, Zhang Lei L, Ge Hongzhang H, Yao Qinghua Q

This study aimed to predict the potential mechanism of Shenling Baizhu San (SBS) against Chemotherapy-induced Intestinal Mucositis (CIM) using an integrated approach combining network pharmacology, molecular docking, and molecular dynamics simulation, with its pharmacological effects and underlying mechanisms validated experimentally. To evaluate the therapeutic effect of SBS on CIM, this study established a CIM rat model using 5-Fluorouracil (5-FU). Subsequently, we conducted a comprehensive evaluation of the model through general observation, histopathological evaluation, ELISA, immunohistochemistry, and immunofluorescence. Based on network pharmacology predictions, we validated the effect of SBS on PI3K-Akt pathway proteins by immunohistochemical staining of colon tissues. In addition, we explored the mechanism of SBS using 16S rDNA sequencing and quantitative analysis of short-chain fatty acids in feces. SBS significantly mitigated CIM induced by 5-FU in rats. Network pharmacology analysis revealed that quercetin and kaempferol are the primary active components of SBS. These compounds exert their effects by acting on core targets such as ESR1, HSP90AA1, and GSK3B, and modulating pathways including PI3K-Akt. Immunohistochemical staining confirmed SBS's inhibitory effect on PI3K and Akt. 16S rDNA sequencing analysis showed that SBS intervention significantly increased the richness and α-diversity of gut microbiota. Quantitative analysis of SCFAs showed that SBS significantly increased the content of acetic, propanoic, butanoic, isobutyric, valeric, isovaleric, and hexanoic acids. The integration of network pharmacology and experimental validation demonstrates that SBS primarily exerts its therapeutic effects against CIM by modulating the PI3K-Akt pathway. Analyses of gut microbiota and metabolism revealed that SBS reduces gut microbiota imbalance and increases SCFA concentrations, which, in turn, aid the recovery of intestinal mucosa damaged by injury. Our findings indicate that SBS is a multi-component agent that acts against CIM by modulating the PI3K-Akt pathway, attenuating gut dysbiosis, and elevating SCFA concentrations. These findings provide a novel mechanistic framework and translational strategy for its clinical application.

PMID 43012134
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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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PubMedHistology and histopathology2026-11-10

Probiotic Lactobacillus reuteri mitigates 5-fluorouracil-induced oral mucositis via suppression of the FTO/CMPK2/NLRP3 pathway.

Qiu Jingcheng J, Chen Zhouhua Z, Chen Tao T, Cao Lu L

5-Fluorouracil (5-FU)-induced oral mucositis (OM) is associated with the fat-tissue-associated protein (FTO)/cytidine monophosphate kinase 2 (CMPK2)/NOD-like receptor protein 3 (NLRP3) inflammatory axis. Lactobacillus reuteri (LR) may protect against 5-FU-induced OM through this pathway, yet the precise mechanism requires clarification. We aimed to investigate whether LR alleviates 5-FU-induced OM by suppressing the FTO/CMPK2/NLRP3 inflammasome pathway. A hamster OM model was established using 5-FU injections and mechanical irritation, with LR administered in drinking water. Macroscopic scoring, histopathology, serum ELISA, and tissue oxidative markers were assessed. Protein expression of FTO, CMPK2, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and pro-caspase-1 was analyzed by western blot. In vitro, human oral keratinocytes (HOKs) were treated with 5-FU, LR, FTO-overexpression transfection (oe-FTO), and/or lipopolysaccharides (LPS). Cell viability, migration, proliferation, ROS, cytokines, and mRNA/protein levels of FTO/CMPK2/NLRP3 were evaluated. LR alone and LPS alone controls were included to rule out direct effects. In hamsters, LR significantly reduced mucosal ulceration (injury score from 3.67 ± 0.52 to 2.50 ± 0.84, p<0.05), inflammatory cell infiltration, mast cell numbers (p<0.01), and serum IL-8, TNF-α, and IL-1β (all p<0.01). LR also ameliorated oxidative stress (decreased MDA, increased SOD) and downregulated FTO, CMPK2, and NLRP3 protein expression (all p<0.01). qPCR confirmed successful LR colonization in the OM of LR-treated hamsters. In HOKs, LR (109 CFU/mL) restored 5-FU+oe-FTO-impaired cell viability (from 45.3±3.8% to 71.5±4.6% at 24h, p<0.01), migration (from 40.2±3.3% to 70.4±3.4%, p<0.01), and proliferation (EdU-positive cells from 29.8±3.0% to 39.9±1.9%, p<0.01). Baseline assessment showed that LR alone enhanced HOK viability and reduced ROS/IL-8/TNF-α (p<0.05), whereas LPS alone reduced viability and elevated ROS/IL-8/TNF-α/IL-1β (p<0.05). FTO overexpression exacerbated 5-FU damage and pathway activation, while FTO knockdown reversed these deficits (migration: from 45.24±4.49% to 62.52±5.59%, p<0.01; EdU: from 32.42±3.08% to 47.44±2.98%, p<0.01). LR suppressed FTO/CMPK2/NLRP3 expression at mRNA and protein levels, and these effects were abolished by the NLRP3 agonist LPS. LR alleviates 5-FU-induced OM by inhibiting the FTO/CMPK2/NLRP3 inflammasome axis, reducing inflammation and oxidative stress. These findings are supported by both overexpression and knockdown experiments, as well as by human-relevant insights into LR-microbiome interactions.

PMID 43004956
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PubMedJournal of surgical oncology2026-11-10

Treatment Response and Oncologic Outcomes Following Neoadjuvant Chemotherapy Switch in Localized Pancreatic Ductal Adenocarcinoma.

Gist Galen C GC, Broderick Joseph C JC, Adams Alexandra M AM, Prakash Laura L et al.

Many patients undergoing neoadjuvant therapy for localized pancreatic ductal adenocarcinoma (PDAC) experience treatment intolerance or disease progression during initial therapy. Although chemotherapy switch is increasingly utilized, response rates and oncologic outcomes remain poorly defined. Patients were identified from a prospectively maintained database of individuals undergoing neoadjuvant therapy for localized PDAC from 2012 to 2023. Eligible patients underwent chemotherapy switch between 5-fluorouracil and gemcitabine regimens with curative intent. Favorable response was defined as complete or partial radiographic response by RECIST, or stable disease with a ≥ 50% decline in CA 19-9 relative to levels before switch. Outcomes were measured from the date of chemotherapy switch. Out of 161 patients, 41% achieved favorable response. Body/tail, borderline resectable, and locally advanced disease were independently associated with nonfavorable response. Among favorable responders, 49% underwent resection versus 11% of nonresponders. Favorable response was independently associated with improved progression-free and overall survival, including among unresected patients. Overall, 47% derived meaningful oncologic benefit through favorable response, resection, or both. Chemotherapy switch offers a reasonable strategy in select patients with localized PDAC experiencing inadequate response or intolerance of initial therapy. This composite response framework identifies chemosensitive tumor biology, informs surgical decision-making, and stratifies prognosis.

PMID 43004806
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