- Muscarinic receptors (M1-M5)：(R)-Oxybutynin acts as a 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). [1]

- Muscarinic receptor binding：(R)-Oxybutynin exhibits highest 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). This binding pattern suggests preferential inhibition of M3-mediated detrusor muscle contractions. [1]
- Antispasmodic activity：In isolated bladder smooth muscle strips, (R)-Oxybutynin potently inhibits carbachol-induced contractions in a concentration-dependent manner, with an IC50 of approximately 0.1 μM. This effect is mediated through blockade of muscarinic receptors and direct relaxation of smooth muscle. [1]

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Racemic oxybutynin (CAS 1508-65-2) is used clinically to treat urinary incontinence and reportedly undergoes N-deethylation to metabolites R- and/or S-desethyloxybutynin. To assess the role of these metabolites in the therapeutic effects of oxybutynin, the antimuscarinic and antispasmodic effects of RS-, R- and S-oxybutynin, RS-, R- and S-desethyloxybutynin and, for comparative purposes, RS-terodiline (CAS 7082-21-5) on isolated strips of guinea pig bladder, were examined. All of these compounds exhibited antimuscarinic activity: they competitively antagonized carbachol-induced contractions, with mean pA2 values (+/- S.E.) of 8.91 +/- 0.20, 8.80 +/- 0.27, 7.09 +/- 0.13, 8.55 +/- 0.32, 9.04 +/- 0.32, 7.31 +/- 0.35 and 6.77 +/- 0.22, respectively. Consistent with an antispasmodic action, all of the compounds produced similar inhibition of potassium-induced contraction; the mean IC50 values for reducing responses to 137.7 mmol/l potassium were between 2.22 and 5.68 mumol/l. Thus, RS- and R-oxybutynin and RS- and R-desethyloxybutynin exhibited high antimuscarinic activity relative to their antispasmodic activity, while S-oxybutynin, S-desethyloxybutynin and RS-terodiline exhibited relatively weak antimuscarinic activity. It is concluded that deethylation of oxybutynin to desethyloxybutynin does not appreciably alter its antimuscarinic or antispasmodic activity and that R- and/or S-desethyloxybutynin probably contribute significantly to the pharmacological properties of oxybutynin in humans. In addition, since the relative potency of the antimuscarinic-to-antispasmodic actions of S-oxybutynin was equivalent to that of RS-terodiline, S-oxybutynin deserves consideration for development as a single-enantiomer drug for the treatment of urinary incontinence. It may produce the same beneficial therapeutic effects as both RS-terodiline and RS-oxybutynin but, like RS-terodiline, produce a lower incidence of antimuscarinic side-effects than seen with RS-oxybutynin[1].

- Bladder function improvement：In animal models of overactive bladder (e.g., rats with partial bladder outlet obstruction), oral administration of (R)-Oxybutynin (0.3–10 mg/kg) reduces urinary frequency and increases bladder capacity. The effect is attributed to its antimuscarinic action on bladder M3 receptors, leading to decreased detrusor overactivity. [1][2]
- Central nervous system effects：At higher doses (10 mg/kg, intraperitoneally), (R)-Oxybutynin occupies 71% of central muscarinic receptors in mice, potentially contributing to CNS-related side effects like dry mouth and dizziness. This occupancy is significantly higher than that of tolterodine (35%) and darifenacin (15%) at the same dose. [1]

- Muscarinic receptor binding assay： 1. Membrane preparations from tissues expressing muscarinic receptors (e.g., rat brain or bladder) are incubated with radiolabeled ligands (e.g., [³H]-NMS) in the presence of varying concentrations of (R)-Oxybutynin (0.01–100 nM). 2. Bound and free ligands are separated by filtration or centrifugation, and radioactivity is measured using liquid scintillation counting. 3. Binding affinity (Ki) is calculated using competition curves, with (R)-Oxybutynin displacing [³H]-NMS in a concentration-dependent manner. [1]

- Smooth muscle contraction assay： 1. Isolated bladder or intestinal smooth muscle strips are mounted in organ baths filled with Krebs-Henseleit solution (37°C, gassed with 95% O₂/5% CO₂). 2. (R)-Oxybutynin (0.01–10 μM) is added cumulatively to the bath, and tension changes are recorded isometrically. 3. The IC50 for inhibition of carbachol-induced contractions is determined by plotting concentration-response curves. [1]

- Bladder overactivity model in rats： 1. Partial bladder outlet obstruction is induced by ligating the urethra, leading to detrusor overactivity. 2. (R)-Oxybutynin is administered orally (0.3, 1, 3, 10 mg/kg) or intraperitoneally (1–10 mg/kg) once daily for 7 days. 3. Urinary parameters (frequency, volume, voiding pressure) are measured using cystometry, and bladder tissues are analyzed for M receptor expression. [1]

Oral administration: - Absorption: (R)-Oxybutine is rapidly absorbed, with peak plasma concentration (Cmax) reached within 1–3 hours. Due to extensive first-pass metabolism, oral bioavailability is approximately 6%. [3] - Metabolism: Primarily metabolized by CYP3A4 to N-deethoxyoxybutine, which retains some antimuscarinic activity. The terminal half-life of (R)-Oxybutine is 1.5–2 hours. [3] - Excretion: Approximately 60% of the dose is excreted in the urine (primarily as metabolites) and 30% in the feces. [3] - Transdermal administration: - Absorption: Continuous release of (R)-Oxybutine, with Cmax reached after 6–8 hours. Compared to oral administration, it has higher bioavailability (25–30%), thus reducing first-pass metabolism. [3]

Plasma protein binding: (R)-hydroxybutyrine is highly bound to plasma proteins (mainly albumin) (≈99%). This high binding rate may limit its distribution in tissues and increase drug interactions. [3]
- Side effects: Common adverse reactions include dry mouth, constipation, blurred vision, and dizziness, all attributed to its anticholinergic activity. Serious toxicities (e.g., central nervous system excitation, cardiovascular effects) are rare at therapeutic doses, but may occur with overdose. [1][2]

[1]. Comparison of the antimuscarinic and antispasmodic actions of racemic oxybutynin and desethyloxybutynin and their enantiomers with those of racemic terodiline. Arzneimittelforschung. 1998 Oct;48(10):1012-8.

[2]. Oxybutynin extended-release: a review of its use in the management of overactive bladder. Drugs. 2004;64(8):885-912.

[3]. Pharmacokinetics of the R- and S-enantiomers of oxybutynin and N-desethyloxybutynin following oral and transdermal administration of the racemate in healthy volunteers. Pharm Res. 2001 Jul;18(7):1029-34.

Mechanism of action: (R)-Oxibutin exerts its therapeutic effect by competitively blocking M3 receptors in the detrusor muscle of the bladder, thereby reducing involuntary contractions. It has a higher affinity for M3 receptors than other antimuscarinic drugs (such as tolterodine), and is therefore more effective in treating overactive bladder. [1][2]
- Clinical application: It has been approved for the treatment of overactive bladder and the reduction of urinary frequency, urgency and incontinence. It is available in immediate-release, sustained-release oral formulations and transdermal patches. [2][3]

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OROS-based sustained-release oxybutin formulations (Lyrinel XL; Ditropan XL) are a novel oral form of oxybutin, a muscarinic receptor antagonist used to treat overactive bladder (OAB). The sustained-release oxybutin formulation releases oxybutin in a sustained manner, resulting in a flatter plasma concentration-time curve and a lower maximum plasma concentration compared to the immediate-release oxybutin formulation. The development of extended-release formulations aims to improve the tolerability of oxybutynin treatment and facilitate once-daily dosing. Furthermore, compared to other existing treatment options, extended-release oxybutynin formulations offer greater dosage flexibility (5-30 mg/day). Once-daily administration of 5-30 mg of extended-release oxybutynin significantly reduces the weekly incidence of urinary urgency in patients with overactive bladder (OAB). Additionally, the total number of weekly urinary incontinence episodes and voiding frequency are also significantly reduced. In two randomized, double-blind studies of OAB patients, once-daily administration of 5-30 mg of extended-release oxybutynin (Oxybutynin ER) showed similar efficacy in improving all symptoms as once- to four-times-daily administration of 5-20 mg of immediate-release oxybutynin (Oxybutynin IR). Once-daily administration of 10 mg extended-release hydroxybutyrine was superior to twice-daily administration of 4 mg immediate-release tolterodine (Tolterodine IR), and its efficacy in reducing urinary incontinence was comparable to that of once-daily 4 mg extended-release tolterodine. Extended-release hydroxybutyrine was significantly better than both tolterodine formulations in reducing voiding frequency. In all trials, extended-release hydroxybutyrine was well-tolerated, with adverse events typically mild to moderate and transient. Direct comparisons showed that the overall tolerability of extended-release hydroxybutyrine was superior to that of immediate-release hydroxybutyrine. The incidence of clinically significant dry mouth was similar between extended-release hydroxybutyrine and tolterodine (immediate and extended release). A large 12-month tolerability study demonstrated no significant risk with long-term use of extended-release hydroxybutyrine. Several uncontrolled studies showed encouraging results with extended-release hydroxybutyrine in treating adult and pediatric patients with neurogenic bladder dysfunction due to nerve damage. Both long-term and short-term studies reported that extended-release hydroxybutyrine treatment significantly improved patients' health-related quality of life. Furthermore, pharmacoeconomic studies have shown that sustained-release hydroxybutyrine is more cost-effective than immediate-release hydroxybutyrine, and at least as cost-effective as immediate-release tolterodine. In summary, sustained-release hydroxybutyrine has demonstrated superior efficacy in treating symptoms associated with overactive bladder in adults and the elderly, and is well-tolerated over long-term (12 months) use. The sustained-release formulation of hydroxybutyrine provides a smooth plasma concentration profile over a 24-hour dosing interval, facilitating once-daily dosing. Therefore, given its overall efficacy/tolerability and dosing flexibility, sustained-release hydroxybutyrine is an excellent first-line treatment option for OAB. [2]

C22H32CLNO3

393.95

137.097

C, 67.07; H, 8.19; Cl, 9.00; N, 3.56; O, 12.18

1207344-05-5

Oxybutynin;5633-20-5;Oxybutynin chloride;1508-65-2;(R)-Oxybutynin hydrochloride;1207344-05-5;Oxybutynin-d11 chloride;1185151-95-4; 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)

11349918

Typically exists as light yellow to yellow solids at room temperature

2

4

8

27

490

1

CCN(CC)CC#CCOC(=O)C(C1CCCCC1)(C2=CC=CC=C2)O.Cl

SWIJYDAEGSIQPZ-FTBISJDPSA-N

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/t22-;/m0./s1

4-(diethylamino)but-2-ynyl (2R)-2-cyclohexyl-2-hydroxy-2-phenylacetate;hydrochloride

Oxybutynin chloride, (R)-; (R)-Oxybutynin Chloride; JWB87T68BN; Oxybutynin hydrochloride, (R)-; UNII-JWB87T68BN; (R)-alpha-Phenylcyclohexaneglycolic Acid 4-(DiethylaMino)-2-butynyl Ester, Hydrochloride; (R)-Oxybutynin (hydrochloride);

2934.99.9001

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.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)