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ticlopidine (Tagren / ticlopidine, KRKA)

✓ Approved

Krka · P2RY12 · 小分子

什么是 ticlopidine？

ticlopidine 是一种小分子，由Krka研发。该药已获批，用于治疗相关适应症。

药物档案

商品名Tagren, ticlopidine, KRKA
公司Krka
药物类别小分子
分子靶点P2RY12
状态Approved
来源： ClinicalTrials.gov, Krka

作用机制

分子靶点

ticlopidine 作用于 1 个分子靶点：

P2RY12purinergic receptor P2Y12 (P2Y(ADP), P2Y(cyc))
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

ticlopidine 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersThrombosis✓ Approved

相关研究文献

PubMedBMJ open2026-08-20

Potentially inappropriate prescribing in Iranian elderly population: a nationwide claims-based analysis.

Kharaghani Mohammad Amin MA, Kianipour Reza R, Ataei Seyed Mohammad-Navid SM, Ebrahimpour Sholeh S et al.

Potentially inappropriate prescribing (PIP) in the elderly is associated with adverse outcomes and increased healthcare use. We aimed to estimate its prevalence and pattern among the elderly population of Iran using the Screening Tool of Older Persons' Prescriptions (STOPP) criteria. Retrospective, population-based observational study. Nationwide data of Iran Health Insurance Organization (IHIO) prescription claims from 24 provinces (21 March 2014 to 19 March 2017). Adults aged ≥60 years with at least one prescription in the dataset were included. The study comprised 2 696 300 older adults who received 28 575 400 prescriptions. Not applicable. Using a two-stage curation process, we selected STOPP version 3 criteria that could be operationalised from dispensing data alone (age, Anatomical Therapeutic Chemical code, dose, duration and concurrent use). For each criterion, we calculated prescription and patient level PIP prevalence overall and among at-risk prescriptions. Across the curated STOPP criteria, 313 315 prescriptions issued to 131 012 patients met at least one PIP criterion. The most frequent PIPs were concurrent beta blocker and diltiazem use (99 027 prescriptions; 1.26% of patients), benzodiazepine therapy ≥4 weeks (89 240 prescriptions; 1.60% of patients), ≥2 anticholinergic drugs (47 079 prescriptions; 0.78% of patients) and concomitant non-steroidal anti-inflammatory drug plus anticoagulant (25 685 prescriptions; 0.38% of patients). PIPs involving acetylcholinesterase inhibitors, ticlopidine, clonidine and methyldopa were rare. In this nationwide claims-based study, about 5% of elderly Iranians were exposed to PIPs, particularly chronic benzodiazepine use, excessive anticholinergic burden and high-risk cardiovascular and antithrombotic combinations. Our findings provide concrete targets for claims-based surveillance and interventions to improve prescribing safety in Iran's ageing population.

PMID 42624577
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PubMedClinical pharmacology and therapeutics2026-08-18

Clinical Significance of Acute Kidney Injury in Idiosyncratic Drug-Induced Liver Injury: A Multicentric Propensity Scores Matched Study.

Pinazo-Bandera José María JM, Niu Hao H, Toro-Ortiz Juan Pedro JP, Medina-Caliz Inmaculada I et al.

Evidence about the role of acute kidney injury (AKI) in idiosyncratic drug-induced liver injury (DILI) is still scarce. We aimed to ascertain the incidence, clinical profile, culprit drugs, and prognosis associated with concomitant DILI and AKI. We include patients from two long-term prospective DILI registries, the Spanish DILI registry and the Latin American DILI (LATINDILI) Network. Demographics, clinical characteristics, and outcome of patients with DILI-AKI were compared to those patients with DILI and without AKI. Overall, 54 out of 978 patients had AKI at the time of DILI diagnosis (5.5%). The most frequent culprit drug implicated in DILI-AKI was amoxicillin-clavulanate (11%) followed by anabolic androgenic steroids, antituberculosis drugs, ebrotidine, and ticlopidine (5.5% each). DILI-AKI cases were older than patients without AKI (60 ± 18 vs. 52 ± 18; P = 0.001), and mostly men (63%; P = 0.022). Furthermore, DILI-AKI cases showed higher comorbidity burden, and cholestatic damage and lymphopenia were more prevalent. Notably, DILI-AKI cases had higher incidence of liver-related death and all-cause mortality than those patients with no renal dysfunction (P = 0.029 and P = 0.015, respectively). In both a multivariable logistic regression (odds ratio [OR] = 3.46; 95% confidence interval [CI] 1.39-8.59; P = 0.008), and a rigorous propensity score-matched analysis (OR = 5.20; 95% CI 1.06-25.52; P = 0.042), renal damage was found as a risk factor of poor outcome. In conclusion, AKI in DILI mostly occurs in older male patients with cholestatic injury, lymphopenia, and greater burden of comorbidities, but mortality is restricted to DILI-AKI patients with hepatocellular damage. Overall, AKI is a risk factor of poor outcome in idiosyncratic DILI.

PMID 42609216
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PubMedJournal of ethnopharmacology2026-08-06

CYP2C19-mediated metabolic activation and OAT3/P-gp-associated transport contribute to Dioscorea bulbifera L.-induced hepatotoxicity.

Tian Yuwei Y, Deng Liping L, Guo Weiyu W, Cheng Zihao Z et al.

Dioscorea bulbifera L. (DBL) is a traditional medicinal herb, but its clinical use is often limited by its potential to cause herb-induced liver injury. 8-Epidiosbulbin E acetate (EEA) is recognized as the major hepatotoxic constituent in DBL; however, the mechanisms underlying the drug transport and metabolic activation of EEA leading to hepatotoxicity are unclear, which severely impedes the understanding of its toxicity risk and safety control measures. This study aimed to identify the key EEA transporters and P450 enzymes mediating EEA metabolic activation in vivo to systematically clarify the contribution of transport and metabolism in DBL/EEA-induced hepatotoxicity. Transporter and P450-overexpressing cell models were used, combined with CCK-8, apoptosis, and cell cycle assays and LC-MS/MS technology, to evaluate EEA cytotoxicity, intracellular content, and EEA-GSH conjugate formation. In animal experiments, mice were pretreated with ticlopidine, probenecid, novobiocin, or verapamil to examine the roles of CYP2C19-mediated metabolic activation, OAT-sensitive uptake, and P-gp-mediated efflux in EEA- and DBL extract-induced hepatotoxicity. EEA or DBL extract was then administered orally, and the extent of liver injury was evaluated by histopathological examination and serum aminotransferase measurements. CYP2C19 metabolically activated EEA, leading to decreased cell viability, increased apoptosis, cell cycle arrest, and increased EEA-GSH conjugate levels. OAT3 overexpression increased EEA cellular uptake, whereas P-gp overexpression promoted EEA efflux. In mice, CYP2C19 or OAT3 inhibition attenuated DBL/EEA-induced liver injury, whereas P-gp inhibition exacerbated hepatotoxicity. These findings suggest that OAT3-sensitive cellular uptake, P-gp-mediated efflux, and CYP2C19-mediated bioactivation are important determinants of EEA hepatotoxicity, which is characterized by GSH depletion, cell-cycle perturbations, and apoptosis. This study provides a mechanistic explanation for DBL/EEA-induced hepatotoxicity and highlights that the interplay between metabolism and transport is a key determinant of its toxicity.

PMID 42556633
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-07-28

Drug-induced microscopic colitis: a systematic review of implicated agents and case-level causality.

Alzahrani Muhanad M, Alabbasi Abdullah A, Alzahrani Ziyad Z, Sayes Mohammed M et al.

Microscopic colitis (MC), including collagenous colitis (CC), lymphocytic colitis (LC) and incomplete MC, is a common cause of chronic watery diarrhoea. Drugs are reported triggers, but observational studies cannot establish individual causality. We reviewed case-level evidence and graded causality using dechallenge/rechallenge criteria. We included published biopsy-confirmed MC case reports and series in which drug exposure preceded symptoms and dechallenge was documented. Data were extracted at the patient level without language or date restriction. Cases were graded as Tier 1 for positive rechallenge or Tier 2 for dechallenge without rechallenge. Quality was assessed using the Murad tool. Twenty-four studies including 69 patients met criteria. Proton-pump inhibitors were most frequent (29/69, 42%), and acid suppressants plus NSAIDs accounted for 36/69 cases (52%). Other agents included ticlopidine, dopaminergic anti-Parkinson drugs, etifoxine, a venotonic, ACE inhibitors and antidepressants. CC and LC were both common. All cases were dechallenge-positive; 11 (16%) had positive rechallenge. Median reported latency was 12 days (range, 5-112). Histology normalised in 22/26 re-biopsied cases. Case-level evidence supports drug-related MC, especially with acid suppressants and NSAIDs. Drug withdrawal remains the key diagnostic and therapeutic step.

PMID 42517880
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PubMedCureus2026-07-17

Antithrombotic Drug Eruptions in Dermatology Practice: Selection Bias, Clinical Phenotypes, and Diagnostic Approaches.

Takada Tomoaki T

Antithrombotic agents are among the most frequently prescribed medications in elderly patients and are essential for the prevention and treatment of cardiovascular and cerebrovascular diseases. Although cutaneous adverse reactions associated with anticoagulants and antiplatelet agents are generally considered uncommon, dermatologists frequently encounter these medications when evaluating patients presenting with pruritic eruptions. This apparent discrepancy may be explained by differences in patient populations. While cardiologists and neurosurgeons manage all patients receiving antithrombotic therapy, dermatologists evaluate a selected population enriched for cutaneous symptoms. This review summarizes the spectrum of cutaneous adverse reactions associated with major antithrombotic agents, including warfarin, heparins, aspirin, ticlopidine, clopidogrel, cilostazol, prasugrel, and direct oral anticoagulants (DOACs). Reported reactions range from common hemorrhagic manifestations to delayed-type hypersensitivity reactions; severe cutaneous adverse reactions, such as drug reaction with eosinophilia and systemic symptoms (DRESS/DIHS), Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), vasculitis, and skin necrosis. Particular emphasis is placed on drug-specific dermatologic phenotypes and diagnostic approaches, including drug-induced lymphocyte stimulation testing, patch testing, and clinicopathological correlation. In addition, Japanese case reports published between 1980 and 2024 are reviewed and integrated with the international literature. These data suggest that antithrombotic agents should not be regarded as a homogeneous dermatologic risk category. Instead, each drug class exhibits characteristic cutaneous reaction patterns that may assist in the differential diagnosis of these reactions in clinical practice. Recognition of these drug-specific phenotypes may facilitate earlier diagnosis, improve interdisciplinary communication, and optimize the management of suspected antithrombotic drug eruptions.

PMID 42465709
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PubMedArchives of toxicology2026-06-15

Metabolism-dependent induction of DNA and chromosome damage by orally administered carbamazepine in adult male C57BL/6J mice, Cyp2b being major activating enzymes.

Sun Haiting H, Chen Manxin M, Zhu Shunda S, Xu Ke K et al.

Carbamazepine is a commonly applied anti-neurosis drug, which meanwhile severely pollutes the global environment. It induced DNA/chromosome damage and gene mutations in vitro following metabolic activation, however, evidence for its genotoxicity in intact mammalians remains absent. In this study, 6-week old male C57BL/6J mice were exposed to carbamazepine by gastric gavage at doses of 8, 20, and 50 mg/kg/d for 7 consecutive days, followed by a micronucleus test in bone marrow polychromatic erythrocytes, a comet assay in hepatocytes, and Western blot assay of hepatic proteins, including a phosphorylated histone 2AX (γ-H2AX, indicator of double-strand DNA breaks), aryl hydrocarbon receptor (AhR), pregnane X receptor (PXR), constitutive androstane receptor (CAR), and several Cyp enzymes. In some experiments, ticlopidine (4 mg/kg/d, specific inhibitor of Cyp2b) was used as a modulator. The results demonstrated no obvious toxicity of carbamazepine to the liver or bone marrow, while it induced micronucleus formation in the bone marrow and hepatic DNA damage (indicated by positive comet assay results and elevated γ-H2AX protein) at 20 and/or 50 mg/kg/d doses, all of which were nevertheless abolished or alleviated by ticlopidine. Meanwhile, carbamazepine induced hepatic AhR and CAR at 50 mg/kg/d, and PXR, Cyp2b10 and Cyp3a11 at doses ≥ 20 mg/kg/d, with no effect on Cyp1a2; furthermore, coexposure of ticlopidine blocked the induction of PXR, Cyp3a11 and Cyp2b10 by carbamazepine, while enhanced that of AhR. This study provides evidence for the genotoxicity of carbamazepine in mammalians in vivo, its dependence on Cyp2b activity, and the activation of relevant nuclear receptor/Cyp-regulating pathway.

PMID 42287383
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