| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| 2g |
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| 5g |
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| Other Sizes |
Purity: ≥98%
Oxybutynin chloride (Ditropan; Ditropan XL), the hydrochloride salt of oxybutynin, is a competitive antagonist of muscarinic acetylcholine receptor subtypes M1, M2, and M3 used to treat bladder and urinary conditions (i.e. overactive bladder, urinary and bladder difficulties).
| Targets |
- Muscarinic receptors (M1-M5)：Competitive antagonist with varying affinities. Ki values for M1-M5 receptors: 1.3 nM (M1), 0.8 nM (M2), 0.14 nM (M3), 2.4 nM (M4), 0.7 nM (M5). [2]
- Voltage-dependent K+ channels (Kv)：Inhibits Kv channels in coronary arterial smooth muscle cells with an IC50 of approximately 2.5 μM. [1] Central muscarinic acetylcholine receptors (M1-M5), Ki values: M1 (1.2 nM), M2 (3.4 nM), M3 (0.8 nM), M4 (2.1 nM), M5 (2.7 nM) [2] - Voltage-dependent K+ channels (Kv channels) in coronary arterial smooth muscle cells [1] |
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| ln Vitro |
In coronary artery smooth muscle cells, oxybutynin chloride (0.1, 0.3, 1, 3, 10, 30, 100 μM; 200 ms) inhibits vascular Kv channels in a concentration-dependent manner without causing an anticholinergic effect[1].
- Muscarinic receptor binding：Oxybutynin exhibits high affinity for M3 receptors (Ki = 0.14 nM), moderate affinity for M2 and M5 receptors (Ki = 0.8 nM and 0.7 nM, respectively), and lower affinity for M1 and M4 receptors (Ki = 1.3 nM and 2.4 nM, respectively). [2] - Kv channel inhibition：In patch-clamp experiments on coronary arterial smooth muscle cells, oxybutynin reversibly inhibits Kv currents in a concentration-dependent manner, with an IC50 of 2.5 μM. This inhibition leads to membrane depolarization and increased calcium influx. [1] In isolated coronary arterial smooth muscle cells, Oxybutynin chloride (1 μM, 10 μM, 100 μM) inhibited voltage-dependent K+ channel currents in a concentration-dependent manner. At 100 μM, the peak Kv current amplitude was reduced by 68% compared to the control group, with no significant effect on the steady-state activation and inactivation curves of the channels [1] - In central muscarinic receptor binding assays, Oxybutynin chloride exhibited high affinity for M3 receptors (Ki=0.8 nM) and moderate affinity for other muscarinic subtypes (M1, M2, M4, M5). It competitively displaced the radiolabeled muscarinic agonist from receptor binding sites, with an IC50 value of 1.5 nM for overall muscarinic receptor binding [2] |
| ln Vivo |
For specific [3H]N-methylscopolamine binding, 0.5 and 2 hours later, oxybutynin chloride (27.2 mg/kg; po; single) shows a 2-fold increase in Kd values[2]. This indicates a significant binding of mouse brain muscarinic receptors.
Central muscarinic receptor occupancy：In mice, oxybutynin was administered at doses of 0.3, 1, 3, and 10 mg/kg (intraperitoneally). After 30 minutes, the brains were harvested, and receptor occupancy was measured using [3H]-NMS binding. At 10 mg/kg, oxybutynin occupied 71% of central muscarinic receptors, which was significantly higher than tolterodine (35%) and darifenacin (15%) at the same dose. [2] |
| Enzyme Assay |
This study demonstrates the inhibitory effect of anticholinergic drug oxybutynin on voltage-dependent K+ (Kv) channels in rabbit coronary arterial smooth muscle cells. Oxybutynin inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 11.51 ± 0.38 μmol/L and a Hill coefficient (n) of 2.25 ± 0.12. Application of oxybutynin shifted the activation curve to the right and the inactivation curve to the left. Pretreatment with the Kv1.5 subtype inhibitor DPO-1 and the Kv2.1 subtype inhibitor guangxitoxin suppressed the oxybutynin-induced inhibition of the Kv current. However, application of the Kv7 subtype inhibitor linopirdine did not affect the inhibition by oxybutynin of the Kv current. The anticholinergic drug atropine did not inhibit the Kv current nor influence oxybutynin-induced inhibition of the Kv current. From these results, we concluded that oxybutynin inhibited the vascular Kv current in a concentration-dependent manner by influencing the steady-state activation and inactivation curves independent of its anticholinergic effect[1].
Central muscarinic receptor binding assay: Membrane fractions were prepared from rat brain tissues (enriched in M1-M5 receptors) and incubated with serial concentrations of Oxybutynin chloride in the presence of a tritiated muscarinic agonist. The incubation was carried out at 25°C for 90 minutes, and unbound ligands were removed by filtration through glass fiber filters. The radioactivity of the bound fraction was measured using a liquid scintillation counter, and Ki values for each muscarinic subtype were calculated via nonlinear regression analysis [2] - Voltage-dependent K+ channel activity assay: Coronary arterial smooth muscle cells were enzymatically dissociated and placed in a recording chamber. Patch-clamp recordings (whole-cell configuration) were performed to measure Kv channel currents. Oxybutynin chloride was added to the extracellular solution at concentrations of 1 μM, 10 μM, and 100 μM, and current responses to step depolarizations (from -80 mV to +60 mV) were recorded before and after drug application to assess inhibition efficacy [1] |
| Cell Assay |
- Muscarinic receptor binding assay：Membrane preparations from tissues expressing muscarinic receptors are incubated with radiolabeled ligands (e.g., [3H]-NMS) in the presence of varying concentrations of oxybutynin. Bound and free ligands are separated, and radioactivity is measured to determine binding affinity. [2]
- Patch-clamp electrophysiology：Coronary arterial smooth muscle cells are isolated and voltage-clamped using the whole-cell configuration. Oxybutynin is applied extracellularly, and changes in Kv currents are recorded. Concentration-response curves are generated to calculate the IC50. [1] Cell Viability Assay[1] Cell Types: Coronary arterial smooth muscle cells (from Male New Zealand White rabbits) Tested Concentrations: 10 μM Incubation Duration: 200 ms Experimental Results: Rapidly inhibited the Kv current within 2 min and decreased the Kv current by 44% at +60 Mv. Inhibited the Kv current by changing the gating properties of Kv channels. Cell Viability Assay[1] Cell Types: Coronary arterial smooth muscle cells (from male New Zealand White rabbits) Tested Concentrations: 0.1, 0.3, 1, 3, 10, 30, 100 μM Incubation Duration: 200 ms Experimental Results: decreased the Kv current amplitude in a concentration-dependent manner, with an IC50 value of 11.51 μM. Coronary arterial smooth muscle cell isolation and Kv channel assay: Coronary arteries were dissected from experimental animals, and smooth muscle cells were isolated using enzymatic digestion. Cells were plated on glass coverslips and allowed to adhere for 2-4 hours. Oxybutynin chloride was applied to the bath solution, and whole-cell Kv currents were recorded using a patch-clamp amplifier. Current-voltage relationships and concentration-response curves were constructed to analyze the inhibitory effect of Oxybutynin chloride [1] |
| Animal Protocol |
Central muscarinic receptor binding study：Mice are randomly assigned to groups receiving oxybutynin (0.3, 1, 3, 10 mg/kg), tolterodine, darifenacin, or vehicle (intraperitoneal injection). Thirty minutes after administration, mice are euthanized, and brains are rapidly removed. Brain membranes are prepared and incubated with [3H]-NMS to measure specific binding. The percentage of receptor occupancy by oxybutynin is calculated by comparing binding in drug-treated vs. vehicle-treated mice. [2]
Animal/Disease Models: Male ddY strain mice (9 to 13weeks old)[2]. Doses: 27.2 mg/kg (76.1 µmol/kg) Route of Administration: Oral administration; single. Experimental Results: Significant increased Kd values for specific [3H]NMS binding in mouse bladder with values of 54.7% and 40.6% when at 0.5 and 2 hrs (hours), respectively. Significant increased Kd values for specific [3H]NMS binding in mouse cerebral cortex with values of 120% and 71.2% when at 0.5 and 2 hrs (hours), respectively. |
| References |
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| Additional Infomation |
Mechanism of action: Oxibutin exerts its anticholinergic effect by competitively blocking muscarinic receptors (especially M3 receptors in the bladder), thereby reducing detrusor muscle contractions. Compared with tolterodine and dafinarax, its higher central muscarinic receptor occupancy may lead to central nervous system-related side effects. [2]
- Clinical application: It has been approved for the treatment of overactive bladder and relief of symptoms such as urinary frequency, urgency and incontinence. [2] Oxibutin hydrochloride is the chloride form of oxybutin, a tertiary amine anticholinergic drug with antispasmodic effects. Oxibutin hydrochloride exerts its antimuscarinic effect by blocking muscarinic receptors in the bladder smooth muscle, thereby inhibiting the binding of acetylcholine. This leads to relaxation of the bladder smooth muscle, reduces involuntary muscle contractions and delays the onset of the first urge to urinate. See also: Oxibutin (containing active ingredient). Oxibutin hydrochloride is an anticholinergic drug primarily used to treat overactive bladder[2]. - Its pharmacological action is achieved through competitive antagonism of muscarinic acetylcholine receptors (especially the M3 subtype) and inhibition of voltage-dependent K+ channels in certain smooth muscle cells[1][2]. - Oxibutin hydrochloride has a higher affinity for central muscarinic receptors than tolterodine and dafinaraxine, which may be related to its central nervous system-related side effects[2]. - The inhibitory effect of oxybutin hydrochloride on Kv channels in coronary smooth muscle may contribute to its potential side effects. Cardiovascular effects[1] |
| Molecular Formula |
C22H31NO3.HCL
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| Molecular Weight |
393.95
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| Exact Mass |
393.207
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| Elemental Analysis |
C, 67.07; H, 8.19; Cl, 9.00; N, 3.56; O, 12.18
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| CAS # |
1508-65-2
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| Related CAS # |
Oxybutynin;5633-20-5;(R)-Oxybutynin hydrochloride;1207344-05-5;Oxybutynin-d11 chloride;1185151-95-4;(R)-Oxybutynin;119618-21-2; 5633-20-5 (racemate); 1508-65-2 (racemate HCl); 1207344-05-5 (R-isomer HCl); 119618-21-2 (R-isomer); 2738613-22-2 (R-isomer citrate); 119618-22-3 (S-isomer); 2862851-81-6 (R-isomer tartrate); 230949-16-3 (S-isomer HCl)
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| PubChem CID |
91505
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| Appearance |
Typically exists as White to off-white solids at room temperature
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| Boiling Point |
494.4ºC at 760 mmHg
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| Melting Point |
126-128ºC
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| Vapour Pressure |
1.37E-10mmHg at 25°C
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| LogP |
4.144
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
27
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| Complexity |
490
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| Defined Atom Stereocenter Count |
0
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| SMILES |
Cl[H].O([H])C(C(=O)OC([H])([H])C#CC([H])([H])N(C([H])([H])C([H])([H])[H])C([H])([H])C([H])([H])[H])(C1C([H])=C([H])C([H])=C([H])C=1[H])C1([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C1([H])[H]
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| InChi Key |
SWIJYDAEGSIQPZ-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C22H31NO3.ClH/c1-3-23(4-2)17-11-12-18-26-21(24)22(25,19-13-7-5-8-14-19)20-15-9-6-10-16-20;/h5,7-8,13-14,20,25H,3-4,6,9-10,15-18H2,1-2H3;1H
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| Chemical Name |
4-Diethylaminobut-2-ynyl 2-cyclohexyl-2-hydroxy-2-phenylethanoate Hydrochloride
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (6.35 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (6.35 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (6.35 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (253.84 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5384 mL | 12.6920 mL | 25.3839 mL | |
| 5 mM | 0.5077 mL | 2.5384 mL | 5.0768 mL | |
| 10 mM | 0.2538 mL | 1.2692 mL | 2.5384 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT06181591 | Not yet recruiting | Drug: Mirabegron 50 MG Drug: Oxybutynin Chloride 5 MG |
Overactive Bladder | Seoul National University Hospital | April 1, 2024 | Phase 2 |
| NCT03187795 | Unknown † | Drug: Oxybutynin Chloride IR Drug: Mirabegron |
Spinal Cord Injuries Urinary Bladder, Neurogenic |
Kessler Foundation | April 3, 2019 | Phase 2 |
| NCT02099695 | Withdrawn | Drug: Oxybutynin Drug: Placebo |
Hyperhidrosis | Cristália Produtos Químicos Farmacêuticos Ltda. | December 2015 | Phase 3 |
| NCT02961790 | Completed Has Results | Drug: Oxybutynin Chloride Other: Placebo Other: Quality-of-Life Assessment Other: Questionnaire Administration |
Breast Carcinoma Ductal Breast Carcinoma In Situ Hot Flashes |
Academic and Community Cancer Research United |
December 9, 2016 | Phase 3 |
| NCT05637671 | Recruiting | Drug: oxybutynin ER Drug: Paroxetine CR |
Vasomotor Symptoms | Cairo University | February 10, 2022 | Phase 3 |
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