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tolterodine (Detrol LA / Detrusitol Neo / Detrusitol Retard)

✓ Approved

Pfizer, Inc. · CHRM1 · Small Molecule

What is tolterodine?

tolterodine is a small molecule developed by Pfizer, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesDetrol LA, Detrusitol Neo, Detrusitol Retard
CompanyPfizer, Inc.
Drug ClassSmall Molecule
Molecular TargetCHRM1, CHRM2, CHRM3, CHRM4
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Pfizer, Inc.

Mechanism of Action

Molecular Targets

tolterodine acts on 4 molecular targets:

CHRM1cholinergic receptor muscarinic 1 (M1, HM1)
CHRM2cholinergic receptor muscarinic 2 (HM2)
CHRM3cholinergic receptor muscarinic 3 (HM3, PBS)
CHRM4cholinergic receptor muscarinic 4 (HM4, M4R)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

tolterodine is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Renal and urinary disordersHypertonic bladder✓ Approved
Renal and urinary disordersUrinary incontinence✓ Approved

Related Research Articles

PubMedMediastinum (Hong Kong, China)2026-09-20

Narrative review: locally advanced thymoma-do we really need induction therapy before extended resection?

Ventura Luigi L

Locally advanced thymoma remains a challenging condition in which complete tumour clearance may require extended surgical resection. Induction therapy, including chemotherapy or chemoradiotherapy, is used in selected patients to improve resectability; however, the evidence supporting its routine use remains limited. This narrative review evaluates the role of induction therapy before extended resection, with particular attention to patient selection, resectability assessment, and multidisciplinary decision-making. A structured narrative review was conducted using PubMed/MEDLINE, supplemented by manual screening of reference lists from relevant articles, reviews, registry analyses, and guideline documents. The original search covered the period from January 1990 to April 2026 and was updated on 21 June 2026 during revision. Search terms included combinations of "thymoma", "thymic epithelial tumours", "locally advanced", "induction therapy", "neoadjuvant treatment", "preoperative chemotherapy", "chemoradiotherapy", "resectability", "borderline resectable", and "extended resection". English-language clinical studies, systematic and narrative reviews, registry analyses, and international guidelines were considered. The available evidence is largely derived from retrospective, heterogeneous studies, often including mixed populations of thymoma and thymic carcinoma. Platinum-based regimens can achieve radiologic response rates of approximately 50-70%, but no prospective or randomised data demonstrate a clear survival advantage over upfront surgery in clearly resectable thymoma. Induction therapy may provide practical advantages in selected anatomically complex or borderline-resectable cases, including tumour bulk reduction, improved operative planning, and potential facilitation of margin-negative resection. However, radiologic response does not necessarily indicate true pathologic downstaging or reduced need for en bloc resection. Current evidence therefore supports a selective, rather than routine, use of induction therapy following multidisciplinary assessment. Extended surgical resection remains the standard of care when complete resection appears achievable upfront. Current evidence is insufficient to support routine induction therapy in clearly resectable locally advanced thymoma, although induction treatment remains appropriate in selected borderline-resectable cases in which preoperative therapy may improve the likelihood or quality of complete resection. Further prospective and collaborative studies are needed to refine patient selection and clarify its role.

PMID 42763646
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PubMedInternational journal of nanomedicine2026-09-20

Glutathione-Responsive Disulfiram Delivery from Thiol-Functionalized N-Doped Carbon Nanodots: An in vitro Proof-of-Concept Study.

Panaei Mohadese M, Mahani Mohamad M, Divsar Faten F, Khakbaz Faeze F

To develop and evaluate a glutathione (GSH)-responsive "Off-On" drug delivery system based on thiol-functionalized N-doped carbon dots (SNCDs) for controlled intracellular release of disulfiram (DSF). SNCDs were synthesized using a solvothermal technique and subsequently characterized using dynamic laser scattering, high-resolution electron imaging, UV-Vis spectrophotometry, and Fourier-transform infrared spectroscopy (FTIR). DSF was immobilized onto SNCDs through redox-cleavable disulfide linkages, and loading efficiency was determined by UV-Vis analysis. The in vitro drug release kinetics were examined under simulated physiological (pH 7.4) and tumor-relevant acidic (pH 5.4) conditions, evaluating the impact of glutathione (GSH) by performing experiments with and without its inclusion. Cytotoxicity and compatibility studies in MCF-7 breast tumor cells, evaluated via MTT test, were used to investigate SNCD biocompatibility and the anticancer performance of DSF-SNCDs. The FTIR spectra confirmed effective thiol functionalization and revealed oxygenated and nitrogenous groups on the particle surface suitable for disulfide linkage formation. DSF loading efficiency reached approximately 75%. Under non-reducing conditions, DSF-SNCDs exhibited minimal premature release (≤30% over 24 h at pH 7.4 and 5.4), demonstrating an "Off" state. In contrast, the presence of 5% (w/v) GSH at pH 5.4 triggered rapid DSF release, achieving approximately 80% cumulative release within 24 h, corresponding to the "On" state through reductive disulfide bond cleavage. Bare SNCDs showed high biocompatibility (>85% cell viability at 50 µg/mL), whereas DSF-SNCDs produced significantly enhanced cytotoxicity under GSH conditions, confirming redox-activated drug release. SNCDs provide an effective GSH-responsive nanoplatform for DSF delivery, combining high drug loading, excellent stability under non-reducing conditions, and efficient intracellular drug release under reductive environments. This strategy minimizes premature drug leakage while enhancing anticancer activity, demonstrating strong potential for cancer therapy.

PMID 42763685
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PubMedJournal of clinical and experimental hepatology2026-09-20

Right-Lateralized Side-to-side Cavo-caval Anastomosis With Right Hepatic Vein-Extended Cavotomy in Deceased-donor Liver Transplantation: Technique Standardization and Early Outcomes.

Solanki Sanket S, Hukkeri Vachan V, Sandhyav Rommel R, Sheikh Quadir Q et al.

Hepatic venous outflow obstruction (HVOO) remains a persistent complication of deceased-donor liver transplantation (DDLT). Established anastomotic approaches modify orifice calibre or clamping strategy but do not address the lateral orientation of the outflow reconstruction relative to the graft's natural position within the right subphrenic space. We describe the right-lateralized side-to-side cavo-caval anastomosis with right hepatic vein-extended cavotomy (STSCCA-RHV). A partial side-biting clamp is applied at the right hepatic vein orifice and a 4-cm cavotomy extended inferiorly along the right lateral inferior vena cava wall, aligning the anastomosis with the graft's natural lie and eliminating the anterior hinge point implicated in midline reconstructions. We report a retrospective cohort of 121 consecutive adults undergoing primary DDLT with STSCCA-RHV, performed by a single unified surgical team across five high-volume centres in India (August 2023-August 2025). The primary outcome was clinically significant, intervention-requiring HVOO within 90 days. Clinically significant HVOO occurred in 2 of 121 recipients (1.6%; 95% confidence interval: 0.2-5.8%). Both cases were salvaged by single-stent endovascular intervention with no graft loss attributable to outflow failure. Veno-venous bypass was not required in any case. Median operative time was 380 min (interquartile range [IQR]; 320-440), and cold ischaemia time was 185 min (IQR: 160-210). Early allograft dysfunction occurred in 5.8%, primary non-function in 1.7% and acute kidney injury (any Kidney Disease: Improving Global Outcomes stage) in 33.9%, with only 3.3% reaching stage 3. None of the 18 unplanned reoperations (14.9%) involved outflow-related indications. Ninety-day patient and graft survival were 90.1% and 89.4%, respectively. The STSCCA-RHV achieved a low HVOO incidence, complete avoidance of veno-venous bypass, and 90-day survival outcomes consistent with contemporary DDLT benchmarks, without additional operative complexity. This anatomy-guided modification to caval reconstruction is technically simple and reproducible and warrants prospective comparative evaluation against standard piggyback and side-to-side techniques.

PMID 42763523
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PubMedInternational journal of nanomedicine2026-09-20

Biotinylated ε-Polylysine-Cyclodextrin-Coated Mesoporous Silica Nanoparticles for Targeted pH-Responsive Baicalin Delivery.

Liao Rongqiang R, Ruan Yi Y, Zhang Ke K, Liu Maoxia M

Baicalin (BAI) is a natural flavonoid with antitumor potential, but its poor water solubility and low bioavailability limit clinical use. Mesoporous silica nanoparticles are promising drug carriers due to their large surface area and tunable pore structure, yet premature drug leakage remains a key challenge. A multifunctional nanoplatform, designated as BPCD@BAI@BMSN, was constructed to enable efficient baicalin loading, pH-responsive gated release, and biotin-mediated active tumor targeting. A novel biotin-ε-polylysine-cyclodextrin (BPCD) conjugate was synthesized via EDCI/NHS coupling and characterized by NMR and GPC. Hollow mesoporous silica nanoparticles (BMSN) were prepared by the Stöber method, surface-modified with benzothiazole. The BPCD conjugate was coated onto the nanoparticle surface via cyclodextrin-benzothiazole host-guest self-assembly. The resulting nanoparticles were characterized by TEM, DLS, zeta potential, FTIR, and TGA. Drug loading, pH-responsive release, cytotoxicity against SMMC-7721 cells, cellular uptake evaluated by confocal microscopy and flow cytometry, and in vivo antitumor efficacy in nude mice were systematically evaluated. BPCD@BAI@BMSN exhibited near-spherical morphology with a particle size of approximately 200 nm, a positive zeta potential of +10 mV, a drug loading of 19.85%, and an encapsulation efficiency of 89.6%. Cumulative baicalin release reached approximately 62% at pH 5.5, whereas only about 6% was released at pH 7.4, confirming acid-triggered gated release. The blank carrier showed no significant cytotoxicity with cell viability above 95%, while drug-loaded nanoparticles exhibited enhanced cytotoxicity at pH 6.8. Biotin-functionalized nanoparticles demonstrated significantly higher cellular uptake and tumor accumulation compared to non-targeted controls. In vivo, BPCD@BAI@BMSN achieved a tumor growth inhibition rate of 72.5% compared to the control group, with no obvious toxicity to major organs observed during the 21-day treatment period. BPCD@BAI@BMSN integrates high drug loading, pH-responsive supramolecular gating, and active tumor targeting into a single nanoplatform, offering a promising strategy for baicalin delivery with enhanced antitumor efficacy and favorable short-term biosafety.

PMID 42763689
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PubMedVeterinary research2026-09-20

Bovine viral diarrhea virus (BVDV) relies on cellular lipid droplet biogenesis and lipolysis to provide energy for viral replication.

Xiong Xiaoran X, Liu Yi Y, Zhu Yaohong Y, Wang Jiufeng J et al.

Bovine viral diarrhea virus (BVDV), one of the most important viral pathogens in cattle, causes serious economic losses due to immunosuppression and persistent infections. Previous studies have shown a tight connection between virus infection and lipid metabolism, particularly in the formation and degradation of lipid droplets (LDs). However, the pathogenic mechanism of BVDV infection and the molecular mechanisms by which viral proteins reprogram lipid metabolism remain unclear. We found that BVDV increased cellular LD accumulation by enhancing the production of new lipids, accelerating exogenous fatty acid uptake, and elevating diacylglycerol acyltransferase (DGAT)-dependent esterification of fatty acids (FAs). The generated LDs subsequently release free fatty acids (FFAs) via adipose triglyceride lipase/hormone-sensitive lipase (ATGL/HSL)-dependent lipolysis. This lipolysis-dependent release of FFAs is accelerated and transferred to mitochondria for oxidation by increasing contact between LDs and mitochondria, thereby promoting viral replication. Furthermore, BVDV core protein targets the surface of LDs, increasing and recruiting fatty acid synthase (FASN) and ATGL to promote LD mobilization. Meanwhile, the core protein interacts with mitochondria, linking mitochondria to LDs and facilitating the release of FAs for efficient fatty acid oxidation. Collectively, this study demonstrates that the BVDV core protein regulates cellular lipid metabolism to support BVDV replication, contributing to understanding the pathogenetic mechanisms by which BVDV interacts with host cells.

PMID 42763408
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PubMedCommunications biology2026-09-20

Beyond ER-Golgi trafficking: unconventional protein secretion as a new design frontier for synthetic secretion switches in mammalian cells.

Shi Bingshun B, Qiu Xinyuan X, Jiang Yongheng Y, Cai Jiabo J et al.

Mammalian gene switches enable programmable cell behavior. However, current switches on transcriptional and translational layers require de novo RNA and protein synthesis, and secreted outputs must additionally undergo folding, post-translational processing, and intracellular trafficking, imposing delays that limit rapid extracellular responses. Rapid secretion-control switches instead act on pre-synthesized proteins by controlling retention, trafficking, storage, or release. Most current platforms exploit the classical endoplasmic reticulum (ER)-Golgi pathway, including engineered stimulus-secretion coupling in specialized secretory cells and ER retention, retrieval-signal cleavage, or synchronized trafficking in general mammalian hosts. Although these strategies improve response kinetics, they remain limited by ER dependence, host-cell specificity, cargo compatibility, basal leakage, and post-release transport delays. Here, we review current secretion-control architectures and highlight unconventional protein secretion as an underexplored source of design principles for positioning regulatory control closer to terminal protein export and expanding the architectures available for mammalian secretion control.

PMID 42763312
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