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

PubMedAME case reports2026-10-14

Complete molecular response of left adrenal metastasis from pancreatic neuroendocrine tumor following stereotactic body radiation therapy: a case report.

Aboujaoude Michael M, Frakes Jessica J, Jeong Daniel D, Hoffe Sarah S et al.

While pancreatic neuroendocrine tumors (PNETs) often metastasize to the liver, adrenal gland involvement is uncommon. Management of adrenal metastases with stereotactic body radiation therapy (SBRT) is not common and outcomes are not well described. We report a case of metastatic PNET to the adrenal gland demonstrating sustained complete molecular response without anatomic resolution following SBRT within a multimodal treatment. A 48-year-old male patient was diagnosed in September 2023 with a well-differentiated grade 1 PNET. Initial imaging revealed an 8.9 cm centrally necrotic pancreatic tumor with diffuse peripancreatic infiltration and a biopsy proven 2.9 cm left adrenal metastasis. The tumor was somatostatin receptor (SSTR) positive (Krenning score 4) and was deemed surgically unresectable. Despite sequential treatment with capecitabine-temozolomide, followed by folinic acid, fluorouracil, and oxaliplatin (FOLFOX) and folinic acid, fluorouracil, and irinotecan (FOLFIRI), the adrenal lesion progressed, enlarging to 6.9 cm × 6.3 cm and demonstrated high-grade transformation to well-differentiated grade 3 (Ki-67 40%) by May 2025. The patient underwent SBRT to the left adrenal metastasis, receiving a total dose of 6,000 cGy in 5 fractions followed by systemic peptide receptor radionuclide therapy (PRRT) with 177Lu-DOTATATE for primary pancreatic disease control. One month after SBRT, post-treatment imaging demonstrated reduction in adrenal lesion size (4.5 cm × 4.0 cm) with complete absence of radiotracer uptake. Follow-up imaging in December 2025 confirmed continued size reduction and persistent absence of SSTR uptake. At nearly 1-year post-SBRT, a repeat 64Cu-DOTATATE positron emission tomography (PET)/computed tomography (CT) scan showed no left adrenal gland hypermetabolic activity consistent with a sustained complete molecular response despite persistent residual lesion size. This case of metastatic PNET to the left adrenal gland achieved complete molecular response without anatomic resolution nearly 1-year following ablative SBRT within a multimodal treatment strategy. SBRT may represent an effective local control strategy and therapeutic bridge in carefully selected patients undergoing multimodal treatment.

PMID 42871396
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PubMedThe oncologist2026-10-14

Durable Response to Vebreltinib in Heavily Pretreated MET-Amplified Intrahepatic Cholangiocarcinoma: A Case Report.

Hang Yingying Y, Bai Lu L, Hsu Hsiquan H, Chen Ying Y et al.

MET amplification, although detected in only 2% to 5% of intrahepatic cholangiocarcinomas (ICC), represents an actionable oncogenic driver. Treatment options after failure of first-line immunochemotherapy remain limited, and clinical data on vebreltinib, a novel highly selective MET inhibitor, in this molecular subset are scarce. A 61-year-old woman with metastatic ICC harboring high-level MET amplification (tissue gene copy number, 26.79) experienced disease progression on first-line durvalumab plus gemcitabine/cisplatin, second-line liposomal irinotecan/fluorouracil plus lenvatinib and durvalumab, radiotherapy, and transarterial chemoembolization. Following a brief period of vebreltinib (200 mg twice daily) plus durvalumab that was interrupted by grade 4 myelosuppression, the patient continued on vebreltinib monotherapy after hematologic recovery. Restaging computed tomography demonstrated a partial response (PR), with carbohydrate antigen 19-9 normalizing (a 99.2% reduction). This response lasted over six months until eventual disease progression. To our knowledge, this is the first report of vebreltinib monotherapy inducing a deep and durable partial response in heavily pretreated, MET-amplified ICC, with the response lasting over six months despite eventual disease progression. This case underscores the critical value of comprehensive molecular profiling after first-line treatment failure to identify actionable drivers such as MET amplification.

PMID 42870395
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PubMedACS pharmacology & translational science2026-10-14

Integrated In Silico and Experimental Insights into Immunomodulatory Toll-Like Receptor 7/8 Agonists with Anticancer Potential.

Kumar Pankaj P, Zargar Zahid Bashir ZB, Singh Suraj Pratap SP, Kumar Kushvinder K et al.

Toll-like receptors (TLRs) are key pattern recognition receptors that play a central role in regulating and bridging both innate and adaptive immune responses. Notably, TLR7 and TLR8 agonists have gained significant attention as promising therapeutic candidates because of their ability to activate immune responses and modulate immune signaling pathways for treating viral infections, autoimmune disorders, and cancer. Despite the growing interest in the area of immunotherapy, there remains a substantial gap in the development of new immunomodulators with improved efficacy and safety profiles. The primary objective of the study was to identify and evaluate newly synthesized TLR7/8 agonists using integrated in silico and in vivo strategies. Computational analyses, including molecular docking, molecular dynamics (MD) simulations, pharmacokinetic-pharmacodynamic profiling, and network pharmacology analysis, revealed favorable binding interactions, stability, drug-like properties, and potential targeting of immune- and cancer-related pathways, specifically those relevant to colorectal cancer. In vitro cytotoxicity assays showed that the TLR7/8 agonists exhibit dose-dependent effects in both colorectal cancer cells and RAW 264.7 macrophages. Additionally, the compounds exhibit minimal hemolytic activity, indicating a low potential for systemic toxicity. Furthermore, the cell migration assay demonstrated that several compounds effectively inhibited cancer cell migration, particularly when combined with 5-fluorouracil (5-FU), suggesting potential anticancer and antimetastatic activity. Overall, these findings integrate molecular-level, system-level, and experimental validation approaches to comprehensively evaluate TLR7/8 agonists as potential immunotherapeutic agents. However, further comprehensive in vitro and in vivo investigation studies are necessary to establish the potential of TLR7/8 agonists for use in cancer immunotherapy.

PMID 42871639
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PubMedAME case reports2026-10-14

A hepatic malignant spindle-cell neoplasm of uncertain lineage clinically favoring sarcomatoid hepatocellular carcinoma: a case report.

Li Haowen H, Li Shengwei S, Yu Maohe M, Wei Xin X et al.

Sarcomatoid hepatocellular carcinoma (SHC) is an uncommon and aggressive variant of primary liver cancer. Its clinical and radiological features are often nonspecific, and it may mimic inflammatory liver lesions. Evidence for unresectable SHC is limited, so management is frequently individualized. A 43-year-old man with chronic hepatitis B presented with recurrent right upper abdominal discomfort and 3 kg weight loss over 1 month. He was provisionally diagnosed with a hepatic abscess at an outside hospital, and percutaneous aspiration and drainage were performed; however, microbiological confirmation and detailed treatment records were unavailable. On admission, he had no fever or jaundice. C-reactive protein (CRP) was elevated, procalcitonin (PCT) was low, serum alpha-fetoprotein (AFP) remained below 12 ng/mL, and liver function was child-pugh class A. Contrast-enhanced computed tomography (CT) showed multiple right hepatic lesions with suspected invasion of adjacent portal vein branches. Magnetic resonance imaging (MRI) demonstrated an irregular heterogeneous mass measuring approximately 88×85 mm. Because the clinicoradiological pattern was not fully consistent with simple infection, ultrasound-guided biopsy was performed. Biopsy revealed a hepatic malignant spindle-cell tumor. The initial pathological report noted limited tissue volume and atypical immunohistochemical expression, making definitive subclassification difficult. After integrated clinicopathological review, the lesion was interpreted as a malignant spindle-cell tumor clinically favoring SHC. The unresectable tumor was treated with transarterial chemoembolization (TACE), hepatic arterial infusion chemotherapy (HAIC) with fluorouracil, leucovorin, and oxaliplatin (FOLFOX), lenvatinib 8 mg orally once daily, and tislelizumab 200 mg every 2 weeks. Adverse events were mainly nausea, vomiting, and right upper quadrant (RUQ) pain. Follow-up imaging showed reduction to approximately 70×58 mm and stable disease by response evaluation criteria in solid tumors (RECIST) 1.1. A hepatic malignant spindle-cell tumor clinically favoring SHC should be considered when a presumed liver abscess has atypical imaging findings, low infectious concordance, suspected vascular involvement, or poor diagnostic coherence. Early biopsy is critical. Multimodal therapy may be feasible in selected unresectable cases, but a single case cannot establish efficacy or define the contribution of each treatment component.

PMID 42871401
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PubMedFrontiers in immunology2026-10-14

Fluoropyrimidine-associated gastrointestinal toxicity: pharmacovigilance reporting signals and in vitro evidence of epithelial injury, barrier impairment, and inflammatory responses.

Luan Xinchi X, Li Xiaoran X, Li Xiaoxuan X, Wang Xuezhe X et al.

Fluoropyrimidines, including 5-fluorouracil (5-FU), capecitabine, tegafur, and trifluridine, are widely used anticancer agents, but their gastrointestinal toxicities remain clinically important. This study characterized fluoropyrimidine-associated adverse-event reporting signals across multiple pharmacovigilance databases and described epithelial-cell responses that may provide experimental context for gastrointestinal toxicity. Adverse-event reports from the US Food and Drug Administration Adverse Event Reporting System (FAERS), Japanese Adverse Drug Event Report database (JADER), and Canada Vigilance Adverse Reaction Database (CVARD) were analyzed using the reporting odds ratio (ROR), proportional reporting ratio (PRR), Bayesian confidence propagation neural network (BCPNN), and empirical Bayes geometric mean (EBGM) approaches. Time to onset (TTO) analysis was limited to FAERS because complete onset information was unavailable in JADER and CVARD. GES-1 gastric epithelial cells and NCM460 colonic epithelial cells were used for acute and 7-day repeated-exposure injury experiments. Additional representative-treatment experiments assessed fluorescein isothiocyanate (FITC)-dextran permeability and relative supernatant interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) levels. Fluoropyrimidines showed gastrointestinal reporting signals with drug-specific reporting patterns. TTO analysis in FAERS showed an overall early-reporting pattern; the distribution of reports between days 181 and 360 was exploratory. In vitro, fluoropyrimidines reduced epithelial viability, increased lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) accumulation and decreased the JC-1 red/green ratio. Epithelial injury was also observed under the 7-day repeated-exposure conditions. Quantitative real-time polymerase chain reaction (qPCR) showed lower TJP1, OCLN, and CDH1 transcript abundance and increased expression of selected epithelial inflammatory-response and extracellular-matrix-remodeling genes. In the functional assays, FITC-dextran permeability and relative supernatant IL-6 and TNF-α levels increased after 5-FU, capecitabine, and trifluridine exposure. This study identifies pharmacovigilance reporting signals and provides experimental evidence that fluoropyrimidine exposure is associated with epithelial injury, impaired barrier function, and epithelial inflammatory responses. The reporting signals do not estimate event frequency in treated populations or establish causality and require confirmation in exposure-adjusted studies.

PMID 42871429
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PubMedCancer treatment and research communications2026-10-13

CAD potentially mediates 5‑fluorouracil resistance in gastric cancer cells via modulation of uridine monophosphate synthetase expression.

Yang Yixin Y, Zhao Na N, Zhang Yang Y, Xie Jisheng J et al.

Gastric cancer (GC) is a malignant tumor originating from the gastric mucosal epithelium. While chemotherapy shows initial efficacy in early treatment, it often leads to tumor drug resistance. Studies indicate that over 90% of cancer patient deaths are associated with chemotherapy resistance. Based on this, we explored the expression significance of the pyrimidine metabolism gene CAD in GC. Bioinformatics analysis revealed that CAD expression correlates with survival duration, clinical characteristics, and the prognosis in GC patients. Drug sensitivity analysis revealed an association between CAD and 5-fluorouracil. Experimental validation demonstrated that CAD expression influences GC cell proliferation, migration, invasion, and apoptosis, with this phenomenon also observed in drug-resistant cells. CAD exhibits positive correlation and co-expression with UMPS. This study confirms the high expression of CAD in GC cells, which may promote malignant phenotype transformation through its interaction with UMPS.

PMID 42868639
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