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ticlopidine (Tagren / ticlopidine, KRKA)

✓ Approved

Krka · P2RY12 · Small Molecule

What is ticlopidine?

ticlopidine is a small molecule developed by Krka. It is approved for therapeutic indications.

Drug Profile

Brand NamesTagren, ticlopidine, KRKA
CompanyKrka
Drug ClassSmall Molecule
Molecular TargetP2RY12
StatusApproved
Sources: ClinicalTrials.gov, Krka

Mechanism of Action

Molecular Targets

ticlopidine acts on 1 molecular target:

P2RY12purinergic receptor P2Y12 (P2Y(ADP), P2Y(cyc))
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved

Related Research Articles

PubMedEuropean journal of drug metabolism and pharmacokinetics2026-09-13

Potential Role of CYP3A4 in Determining In Vivo Exposure to Cannabidiol (CBD) and its Active Metabolite 7-OH-CBD: Evidence from an In Vitro Study.

Jaisupa Nattapon N, Birgersson Sofia S, Ashton Michael M

Plasma concentration of cannabidiol (CBD) is a determining factor for its antiseizure efficacy. Since CBD bioavailability decreases with increasing dose, pharmacokinetic drug-drug interactions that reduce its metabolic clearance may represent an alternative strategy to increase systemic exposure without further dose escalation. To investigate in vitro how combinations of antiseizure medications (ASMs) with varying cytochrome P450 (CYP450) inhibitory properties influence the metabolism of CBD and 7-OH-CBD. CBD was incubated with human liver microsomes (HLMs) either alone or in the presence of combinations of two to four commonly prescribed ASMs. These ASMs included valproic acid, clobazam, stiripentol, topiramate, zonisamide, felbamate, perampanel, ethosuximide, rufinamide, lamotrigine, levetiracetam and gabapentin. CBD, 7-OH-CBD and 7-COOH-CBD concentrations were quantified at eight time points by high performance liquid chromatography coupled to tandem mass spectrometry (HPLC-MS/MS). Depletion kinetics, metabolite formation rates, and in vitro intrinsic clearance (CLint) were determined. Ketoconazole, ticlopidine and sulfaphenazole were included as positive controls for CYP3A4, CYP2C19 and CYP2C9 inhibition, respectively. Ketoconazole markedly reduced the CLint of both CBD and its active metabolite, 7-OH-CBD. In contrast, CYP2C19 and CYP2C9 inhibitors produced only minor reductions in CBD CLint. Co-incubation with four CYP3A4-substrate ASMs resulted in a greater reduction in 7-OH-CBD CLint than in CBD CLint. Stiripentol also substantially decreased CBD CLint and markedly reduced the formation of both 7-OH-CBD and 7-COOH-CBD. ASMs with CYP3A4-inhibitory potential may alter systemic exposure to both CBD and its active metabolite, 7-OH-CBD, as demonstrated in vitro. However, co-administration of CBD with CYP3A4-substrate ASMs or CYP2C19 inhibitors is predicted to result in only modest increases in CBD exposure.

PMID 42728549
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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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