- 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)-Oxybutynin is rapidly absorbed, with peak plasma concentrations (Cmax) reached within 1–3 hours. Oral bioavailability is approximately 6% due to extensive first-pass metabolism. [3]
- Metabolism：Primarily metabolized by CYP3A4 to N-desethyloxybutynin, which retains partial antimuscarinic activity. The terminal half-life of (R)-Oxybutynin is 1.5–2 hours. [3]
- Excretion：Approximately 60% of the dose is excreted in urine (mainly as metabolites), and 30% in feces. [3]
- Transdermal administration： - Absorption：Delivers a sustained release of (R)-Oxybutynin, with Cmax achieved after 6–8 hours. Bioavailability is higher (25–30%) compared to oral administration, reducing first-pass metabolism. [3]

- Plasma protein binding：(R)-Oxybutynin is highly bound to plasma proteins (≈99%), primarily albumin. This high binding may limit its distribution to tissues and increase drug-drug interactions. [3]
- Side effects：Common adverse effects include dry mouth, constipation, blurred vision, and dizziness, attributed to antimuscarinic activity. Severe toxicity (e.g., CNS excitation, cardiovascular effects) is 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)-Oxybutynin exerts its therapeutic effects by competitively blocking M3 receptors in the bladder detrusor muscle, reducing involuntary contractions. Its higher M3 affinity compared to other antimuscarinics (e.g., tolterodine) contributes to improved efficacy in overactive bladder. [1][2]
- Clinical use：Approved for the treatment of overactive bladder syndrome, reducing urinary frequency, urgency, and incontinence. Available in immediate-release, extended-release oral formulations, and transdermal patches. [2][3]

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The OROS-based oxybutynin extended-release (ER) formulation (Lyrinel XL; Ditropan XL) represents a new form of oral delivery for oxybutynin, a muscarinic receptor antagonist used in the treatment of overactive bladder (OAB). The release of oxybutynin from oxybutynin ER occurs in a sustained manner, resulting in a smoother plasma concentration-time profile and a lower maximum plasma concentration than those seen with oxybutynin immediate-release (IR). The ER formulation has been developed with the aim of improving the tolerability of oxybutynin therapy and facilitating once-daily administration. Moreover, oxybutynin ER offers greater flexibility in dosage (5-30 mg/day) than the other available treatment options. At dosages of 5-30 mg once daily, oxybutynin ER produced significant decreases from baseline in weekly urinary urge incontinence in patients with OAB. In addition, there were significant decreases in weekly total incontinence episodes and micturition frequency. In two randomised, double-blind studies in patients with OAB, the improvement in all the symptoms with once-daily oxybutynin ER 5-30 mg/day was similar to that produced by oxybutynin IR 5-20 mg/day given one to four times daily. Once-daily oxybutynin ER 10 mg was superior to tolterodine IR 4 mg/day given as two daily doses and as effective as once-daily tolterodine ER 4 mg/day in decreasing urinary incontinence; the decreases in micturition frequency with oxybutynin ER were significantly greater than those seen with either of tolterodine formulations. Oxybutynin ER was well tolerated in all the trials, with adverse events usually being mild to moderate and transient. In direct comparisons, the overall tolerability profile of oxybutynin ER was better than that of oxybutynin IR. Oxybutynin ER was similar to tolterodine (IR and ER) with respect to the incidence of clinically important dry mouth. A large 12-month tolerability study demonstrated no significant risks associated with the long-term use of oxybutynin ER. A few noncomparative studies have shown promising results with oxybutynin ER in the treatment of adult and paediatric patients with neurogenic bladder dysfunction secondary to neuronal injury. Long- and short-term studies have reported significant improvements in health-related quality of life with oxybutynin ER therapy. In addition, pharmacoeconomic studies have suggested that oxybutynin ER is more cost effective than oxybutynin IR and at least as cost effective as tolterodine IR. In conclusion, oxybutynin ER shows excellent efficacy in the treatment of symptoms associated with OAB in adults and the elderly with a good tolerability profile over a prolonged period of use (12 months). The ER formulation of oxybutynin provides a smooth plasma concentration profile over the 24-hour dosage interval, facilitating once-daily administration. Hence, given its overall efficacy/tolerability profile and dosage flexibility, oxybutynin ER provides an excellent treatment option in the first-line pharmacotherapy of 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.)