Fesoterodine L-mandelate is a competitive antagonist of muscarinic acetylcholine receptors (mAChRs). It exhibits high affinity for all five muscarinic receptor subtypes (M1-M5) with pKi values of 8.0, 7.7, 7.4, 7.3, and 7.5 for M1, M2, M3, M4, and M5 receptors, respectively. As a non-subtype-selective antagonist, it does not show significant selectivity among the five subtypes. The primary therapeutic target for the treatment of overactive bladder is the M3 muscarinic receptor subtype, which mediates smooth muscle contraction in the detrusor muscle of the bladder wall. In the bladder, activation of M3 receptors by acetylcholine (released from parasympathetic nerves) leads to contraction of the detrusor smooth muscle, resulting in bladder emptying. By antagonizing M3 receptors in the bladder, fesoterodine (via its active metabolite 5-HMT) reduces abnormal, involuntary detrusor contractions, thereby increasing bladder capacity and reducing symptoms of OAB. Fesoterodine L-mandelate is a prodrug; after oral administration, it is rapidly and completely hydrolyzed to the active metabolite 5-hydroxymethyl tolterodine (5-HMT, which is actually the same active metabolite as that of tolterodine, another antimuscarinic OAB drug). The parent compound fesoterodine itself is essentially inactive, and the pharmacological activity is attributable entirely to the active metabolite 5-HMT. 5-HMT shows some degree of selectivity for bladder M3 receptors over salivary gland M3 receptors, although it is not highly selective, contributing to the common side effect of dry mouth. The L-mandelate salt form does not alter the pharmacological activity but influences the physicochemical properties (solubility, stability, crystallinity) of the drug substance.

Fesoterodine L-mandelate increases the volume of urine produced during a voiding while decreasing the frequency, intensity, and duration of urge incontinence episodes [1]. Following oral ingestion, non-specific esterases quickly and thoroughly hydrolyze fesoterodine L-mandelate in plasma to produce desfesoterodine (5-hydroxymethyl tolterodine; SPM 7605; the active metabolite of fesoterodine).[3][4].

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In vitro functional assays demonstrate that the active metabolite of fesoterodine, 5-hydroxymethyl tolterodine (5-HMT), is a competitive antagonist of muscarinic receptors in bladder tissue preparations. In isolated guinea pig or rat detrusor smooth muscle strips, 5-HMT produces concentration-dependent rightward shifts of the concentration-response curve to the muscarinic agonist carbachol, with Schild plot analysis yielding pA2 values consistent with competitive antagonism. The functional antagonist potency (pA2 or IC₅0) for inhibiting carbachol-induced contraction in isolated bladder strips is in the nanomolar range. The compound does not have intrinsic agonist activity (i.e., it does not cause contraction itself). In radioligand binding assays using membrane preparations from cells expressing individual human muscarinic receptor subtypes (M1-M5), 5-HMT binds with high affinity (Ki in the low nanomolar range). Detailed in vitro data for the L-mandelate salt form of the prodrug itself (as opposed to the active metabolite) are less frequently reported because the prodrug is rapidly converted to 5-HMT in plasma and tissue homogenates. The primary in vitro assays, therefore, are conducted with the active metabolite 5-HMT. However, the rapid conversion can be demonstrated by incubating fesoterodine (including the L-mandelate salt) in plasma or esterase-containing buffer and measuring the appearance of 5-HMT by LC-MS. Fesoterodine L-mandelate decreases micturition frequency, urgency severity, and urgency incontinence episodes, and increases the volume voided with each micturition in functional models. The in vitro activity of fesoterodine L-mandelate as a prodrug is defined by its rapid esterase-mediated conversion to the active metabolite rather than intrinsic receptor binding.

At the lowest studied dose of 0.01 mg/kg, fesoterodine L-mandelate (0.01-1 mg/kg; IV) decreases micturition pressure and increases bladder capacity and ICI (intercontraction interval) [3].

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In vivo, fesoterodine L-mandelate exhibits the pharmacological effects expected of an M3 muscarinic receptor antagonist in the urinary bladder. In rodent models of bladder function (e.g., awake, conscious rats or mice undergoing cystometry), oral or intravenous administration of fesoterodine results in increased bladder capacity, increased intercontraction interval, and reduced micturition pressure without affecting the amplitude of individual bladder contractions. The compound decreases micturition frequency, reduces the severity and frequency of urgency episodes, and decreases episodes of urgency incontinence (involuntary leakage associated with a sudden, strong desire to void). It increases the volume voided with each micturition (voided volume). These effects are consistent with a reduction in detrusor overactivity (unstable bladder contractions). In animal models of overactive bladder induced by various means (e.g., partial bladder outlet obstruction, cerebral infarction, or chemical irritation), fesoterodine dose-dependently restores normal bladder function. The onset of action is relatively rapid following oral administration due to the rapid hydrolysis of the prodrug. The in vivo effects are primarily mediated by the active metabolite 5-HMT. Fesoterodine L-mandelate is used clinically for the treatment of overactive bladder (OAB) symptoms in humans, and its clinical efficacy has been demonstrated in multiple randomized, placebo-controlled clinical trials. The compound's in vivo activity has also been characterized in dogs, rabbits, and other preclinical species as part of the drug development program. The separation between efficacy in the bladder (desired) and effects in salivary glands (dry mouth, the most common adverse effect) reflects the relative distribution and perhaps subtle receptor differences, but the metabolite 5-HMT does not have absolute M3 selectivity, so dry mouth is a predictable side effect. The L-mandelate salt does not alter the in vivo activity profile of the prodrug but enhances the chemical and physical properties for solid dosage form (tablet) manufacturing. In clinical practice, fesoterodine fumarate is another salt form used in some formulations (the L-mandelate salt is a research-grade material).

For in vitro receptor binding assays to determine binding affinity for muscarinic receptor subtypes, cell membrane homogenates from CHO (Chinese hamster ovary) or HEK293 cells stably expressing the individual human muscarinic receptor subtypes (M1, M2, M3, M4, M5) are prepared. Radioligand binding is performed using the non-selective muscarinic antagonist [3H]N-methylscopolamine ([3H]NMS) or [3H]QNB (quinuclidinyl benzilate) as the radioligand. Fesoterodine L-mandelate's active metabolite, 5-hydroxymethyl tolterodine (5-HMT), is used as the test compound (since the prodrug itself has negligible receptor binding affinity). Membrane preparations (10-50 microg protein/well) are incubated with 0.1-1 nM [3H]NMS or [3H]QNB and varying concentrations of unlabeled 5-HMT (10-¹¹ M to 10-⁴ M) in binding buffer (e.g., 50 mM Tris-HCl, pH 7.4, 5 mM MgCl2, 1 mM EDTA, 0.1% BSA) at room temperature or 25degC for 60-120 minutes. Non-specific binding is determined in the presence of 1-10 microM atropine (a classical non-selective muscarinic antagonist) or 10 microM unlabeled 5-HMT. Bound radioactivity is separated by rapid vacuum filtration through GF/B glass fiber filters pre-soaked in 0.3-0.5% polyethyleneimine (PEI) to reduce non-specific binding. Filters are washed three times with ice-cold binding buffer, and retained radioactivity is measured by liquid scintillation counting. Competitive binding curves are generated, and Ki values are calculated from IC₅0 using the Cheng-Prusoff equation: Ki = IC₅0 / (1 + [L]/Kd), where [L] is the concentration of radioligand and Kd is its dissociation constant for the receptor. Assays are typically performed in duplicate or triplicate. Saturation binding experiments can also be conducted to determine the Kd of the radioligand. Reference compounds such as atropine, tolterodine, or oxybutynin are used as positive controls. For functional antagonism assays (e.g., calcium mobilization or IP accumulation), cells expressing individual muscarinic receptor subtypes (coupled to Gq for M1, M3, M5 or Gi for M2, M4) are used. For Gq-coupled receptors (M1, M3, M5): Cells are loaded with a calcium-sensitive fluorescent dye (e.g., Fluo-4-AM). The muscarinic agonist carbachol (EC₈0 concentration, determined from a preliminary concentration-response curve) is used to stimulate calcium mobilization. Increasing concentrations of 5-HMT are added 10-15 minutes before agonist addition. Fluorescence is measured, and the antagonist potency is expressed as pIC₅0 or pKb (the negative logarithm of the equilibrium dissociation constant for the antagonist). Schild plot analysis can be performed by measuring the effect of 5-HMT at several concentrations on the agonist concentration-response curve to confirm competitive antagonism (rightward shift with no suppression of maximum response). For Gi-coupled receptors (M2, M4): functional assays measuring inhibition of forskolin-stimulated cAMP accumulation can be used. Cells are pre-incubated with 5-HMT and then stimulated with carbachol in the presence of forskolin (to activate adenylyl cyclase). cAMP levels are measured by a competitive immunoassay (ELISA). Antagonism results in reduced inhibition of cAMP accumulation. For in vitro assessment of prodrug conversion: Fesoterodine L-mandelate (1-10 microM) is incubated with human plasma, rat plasma, or purified esterases (e.g., butyrylcholinesterase, carboxylesterase) in PBS (pH 7.4) at 37degC for various time points (0-60 minutes). At each time point, an aliquot is mixed with an equal volume of ice-cold acetonitrile containing an internal standard to stop the reaction. After centrifugation, the supernatant is analyzed by LC-MS/MS to quantify the concentrations of fesoterodine (remaining) and the active metabolite 5-HMT (formed). The half-life of fesoterodine conversion is calculated, and the enzyme kinetics (Km, Vmax) of hydrolysis can be determined.

For in vitro cellular pharmacology assays to assess muscarinic receptor antagonism in physiologically relevant cell types, primary human bladder smooth muscle cells (HBSMCs) are cultured in smooth muscle growth medium. Cells are seeded in 96-well plates (10,000-20,000 cells/well) and allowed to reach 80-90% confluence. Cells are serum-starved overnight before the experiment. For calcium mobilization assays: Cells are loaded with Fluo-4-AM (2-5 microM) in HBSS buffer containing 20 mM HEPES and 2.5 mM probenecid (to reduce dye leakage) for 30-60 minutes at 37degC. After washing, cells are incubated with varying concentrations of the active metabolite 5-HMT (or fesoterodine L-mandelate as a control, but note that conversion may occur in the medium due to esterases in serum or secreted by cells; if the assay medium contains serum, the prodrug will be converted to 5-HMT, and the signal will reflect the active metabolite regardless of which form is added) for 10-15 minutes. Calcium flux is then stimulated by addition of carbachol (EC₈0, e.g., 1-10 microM). The fluorescence signal (excitation 488 nm, emission 520-530 nm) is measured in real-time using a fluorescence plate reader (FlexStation, FLIPR, or similar). Antagonist potency is expressed as pIC₅0 for inhibition of the carbachol-induced calcium peak. For cell viability and toxicity assessment: cells are treated with the compound (0.1-100 microM) for 24-72 hours, and viability is measured using MTT, WST-1, or CellTiter-Glo assays. For muscarinic receptor internalization studies: HBSMCs or CHO-M3 cells are treated with 5-HMT (10 nM-1 microM) in the presence or absence of carbachol (1-10 microM). After 15-60 minutes, cells are fixed, permeabilized, and stained with an anti-M3 receptor antibody (or anti-flag tag if using tagged receptors) followed by a fluorescent secondary antibody. Receptor localization (membrane vs. intracellular) is visualized by confocal microscopy, and the degree of internalization is quantified by image analysis. Since fesoterodine is a prodrug, it is generally the active metabolite 5-HMT that is used in cell-based assays to avoid variability in esterase-mediated conversion. However, for studies of prodrug conversion, the conversion of fesoterodine to 5-HMT in cell culture medium (which contains serum esterases) can be monitored by collecting medium at various time points and analyzing by LC-MS.

Animal/Disease Models: Female SD (SD (Sprague-Dawley)) rat bladder (225-275 g) [3]
Doses: 0.01, 0.1 and 1 mg/kg
Route of Administration: intravenous (iv) (iv)injection
Experimental Results: At the lowest dose tested, micturition pressure diminished, bladder Capacity and ICI increased by 0.01 mg/kg.

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For in vivo efficacy studies in animal models of overactive bladder (OAB), several well-established models are used to evaluate the effects of fesoterodine L-mandelate. Model 1 - Awake, conscious rat cystometry (most common model): Female Sprague-Dawley rats (200-300 g) are anesthetized with isoflurane. A lower midline abdominal incision is made, and the urinary bladder is exposed. A polyethylene catheter (PE-50) with a flared tip is implanted into the bladder dome through a small incision, secured with a purse-string suture, and tunneled subcutaneously to exit at the back of the neck. The catheter is plugged when not in use. The abdominal incision is closed. After a recovery period of 3-7 days, the rat is placed in a metabolic cage with a swivel attachment for the catheter. The bladder catheter is connected via a three-way stopcock to an infusion pump and a pressure transducer. Continuous cystometry is performed by infusing warm sterile saline (or a urothelial irritant such as 0.1% acetic acid to induce OAB symptoms) into the bladder at a rate of 50-100 microL/min. Intravesical pressure is recorded continuously using data acquisition software (e.g., PowerLab, Biopac). Standard cystometric parameters are measured: (1) micturition pressure (peak voiding pressure, measured in cmH2O), (2) threshold pressure (pressure at which micturition is initiated), (3) baseline pressure (resting intravesical pressure), (4) intermicturition interval (time between voiding contractions, in minutes), (5) bladder capacity (volume infused to reach micturition threshold, in mL), (6) voided volume (volume expelled during voiding, measured by collecting urine in a funnel placed under the cage connected to a fraction collector or by weighing). After establishing a stable baseline (30-60 minutes), fesoterodine L-mandelate is administered orally (by gavage) at doses of 0.1-3 mg/kg (or as the active metabolite equivalent) in a vehicle such as 0.5% methylcellulose or water. Cystometry continues for 2-4 hours after dosing. The effect of the compound is expressed as the percent change from baseline in bladder capacity, intermicturition interval, and micturition pressure. A positive effect is an increase in bladder capacity and intermicturition interval (indicating increased storage function) with a decrease in micturition pressure (reduced voiding contraction force). An effective antimuscarinic agent reduces bladder overactivity. Control animals receive vehicle only. For studies of oral bioavailability or dose-response, multiple dose groups are used. The L-mandelate salt is compared to other salt forms (e.g., fumarate) or to the standard drug tolterodine as a positive control. Model 2 - Partial bladder outlet obstruction (PBOO)-induced bladder overactivity in rats (surgical model of OAB): Male rats undergo surgical partial ligation of the urethra (silver wire or suture placed around the proximal urethra with a standard diameter rod inserted to control the degree of obstruction). After 4-6 weeks, the rats develop bladder hypertrophy and detrusor overactivity, as confirmed by cystometry. Fesoterodine L-mandelate is then administered, and cystometry is performed as described above. This model more closely mimics clinical OAB due to obstruction (e.g., benign prostatic hyperplasia). Model 3 - Cerebral infarction-induced bladder overactivity in rats (central nervous system model): The middle cerebral artery is occluded (MCAO) in rats to produce a cortical infarct, leading to neurogenic detrusor overactivity. Fesoterodine is administered orally for several days, and conscious cystometry is performed. This model mimics OAB following stroke. Model 4 - Acetic acid-induced bladder overactivity in mice: Female mice (20-25 g) are anesthetized. A catheter is inserted into the bladder via the urethra or surgically implanted. Continuous cystometry is performed as described for rats. Bladder overactivity is induced by adding 0.1-0.5% acetic acid to the infusion saline. Fesoterodine L-mandelate is administered orally (0.1-3 mg/kg) 30-60 minutes before the start of infusion. In all models, at the end of the experiment, animals are euthanized, bladders are excised and weighed (to assess hypertrophy), and bladder tissue may be processed for histology or for ex vivo contractility studies (isometric tension recording in organ baths to measure responses to carbachol, electrical field stimulation, and the effect of 5-HMT on these responses). For assessment of salivary gland effects (dry mouth), a common side effect of antimuscarinic drugs, anesthetized rats can be treated with fesoterodine L-mandelate (orally), and saliva production is measured by placing pre-weighed cotton balls in the mouth for a defined period (5-10 minutes), then re-weighing to determine the weight of saliva absorbed. The ratio of bladder effects (increase in bladder capacity) to salivary effects (decrease in salivation) is used as a measure of bladder selectivity. As expected, fesoterodine shows some selectivity for bladder over salivary glands compared to older antimuscarinic drugs but not absolute selectivity (dry mouth remains the most common adverse effect).

Pharmacokinetic properties of fesoterodine L-mandelate are defined primarily by its behavior as a prodrug. After oral administration, fesoterodine (as the L-mandelate salt or other salt forms such as fumarate) is rapidly and extensively absorbed from the gastrointestinal tract. The drug undergoes immediate and complete hydrolysis by non-specific esterases in the intestinal wall and plasma to form the active metabolite, 5-hydroxymethyl tolterodine (5-HMT). Due to this rapid first-pass metabolism (presystemic hydrolysis), the parent compound fesoterodine is not detectable (or is present only at very low, transient concentrations) in the systemic circulation following oral administration. Consequently, the pharmacokinetics of fesoterodine are defined by the active metabolite 5-HMT. The bioavailability of 5-HMT is approximately 50-60% following oral administration of fesoterodine (the exact value depends on the salt form and formulation). The Tmax (time to reach peak plasma concentration) of 5-HMT is typically 1-2 hours post-dose. The terminal elimination half-life of 5-HMT is approximately 7-8 hours in humans, allowing once-daily dosing. Steady-state concentrations are achieved within 3-5 days of repeated once-daily dosing. The volume of distribution of 5-HMT is large (approximately 200-300 L), indicating extensive tissue distribution, consistent with the lipophilic nature of the metabolite. Plasma protein binding of 5-HMT is high (approximately 90%), primarily to albumin and alpha1-acid glycoprotein (AAG). The metabolism of 5-HMT occurs via two primary pathways: (1) glucuronidation by UDP-glucuronosyltransferase (UGT) enzymes (primarily UGT2B7) to form a glucuronide conjugate that is excreted in urine; (2) oxidative metabolism (CYP2D6-dependent) to form inactive carboxy metabolites. Approximately 35% of the dose is excreted in urine as glucuronide conjugates of 5-HMT, and about 20% is excreted as the carboxy metabolite; the remainder is excreted in feces (likely via biliary excretion). In poor metabolizers of CYP2D6 (a genetic polymorphism), the half-life of 5-HMT may be slightly prolonged (approximately 9-10 hours) and exposure may be increased (~1.5- to 2-fold) because the oxidative pathway is impaired, but this is not considered clinically significant for fesoterodine (unlike for tolterodine, where the dose is adjusted in CYP2D6 poor metabolizers). Fesoterodine‘s metabolism is less dependent on CYP2D6 because the major pathway is via non-specific esterase hydrolysis to 5-HMT, which is the same active metabolite for both rapid and poor CYP2D6 metabolizers; the subsequent metabolism of 5-HMT is partially CYP2D6-dependent, but the effects of poor metabolizer status are modest. The linearity of pharmacokinetics has been demonstrated over the therapeutic dose range (4-8 mg once daily). Food has no significant effect on the absorption or exposure of 5-HMT (i.e., can be taken without regard to meals). The L-mandelate salt is a solid form (crystalline powder) suitable for tablet formulation, but the PK properties are primarily determined by the active metabolite 5-HMT after hydrolysis, regardless of the specific salt form of the prodrug (provided the salt is water-soluble and the prodrug is absorbed). The parent drug fesoterodine is designed to achieve rapid, consistent, and complete conversion to 5-HMT. The L-mandelate salt influences the rate of dissolution and solubility of the drug substance, but the overall oral bioavailability and PK are generally similar to other salt forms (e.g., fumarate) when the dissolution rate is not rate-limiting in vivo. Detailed species-specific PK parameters (in rats, dogs) have been reported in the literature as part of fesoterodine development, but these are not detailed in standard supplier datasheets.

[1]. Fesoterodine for the treatment of urinary incontinence and overactive bladder. Ther Clin Risk Manag. 2009;5:869-76. Epub 2009 Nov 18.

[2]. The Beneficial Effect of Fesoterodine, a Competitive Muscarinic Receptor Antagonist on Erectile Dysfunction in Streptozotocin-induced Diabetic Rats.

[3]. Pharmacological Characterization of a Novel Investigational Antimuscarinic Drug, Fesoterodine, in Vitro and in Vivo. BJU Int. 2008 Apr;101(8):1036-42.

[4]. Fesoterodine: A Novel Muscarinic Receptor Antagonist for the Treatment of Overactive Bladder Syndrome. Expert Opin Pharmacother. 2008 Jul;9(10):1787-96.

Fesoterodine L-mandelate is the active pharmaceutical ingredient (API) of a clinically approved drug (marketed under various brand names including Toviaz, as the fumarate salt). The fumarate salt is used in approved pharmaceutical products (tablets) for the treatment of overactive bladder (OAB) with symptoms of urge urinary incontinence, urgency, and frequency. The L-mandelate salt form is a research-grade chemical standard used for analytical and preclinical investigations. The safety profile of fesoterodine is well-established based on extensive clinical trials and post-marketing experience. Common adverse effects in humans include dry mouth (the most frequent, occurring in approximately 20-30% of patients), constipation, dyspepsia (indigestion), nausea, abdominal pain, dry eyes, blurred vision (due to M3 antagonism in the ciliary muscle of the eye, causing cycloplegia and difficulty focusing on near objects), dizziness, headache, fatigue, urinary retention (paradoxical, due to excessive bladder muscle relaxation, but this is rare at therapeutic doses), and increased heart rate (tachycardia, due to antagonism of M2 receptors in the heart which normally inhibit sympathetic tone; the heart rate increase is usually modest at therapeutic doses of ~5-10 mg/day but can be more pronounced with higher doses or in susceptible individuals). Less common adverse effects include cognitive impairment (especially in elderly patients; muscarinic antagonists can cross the blood-brain barrier to varying degrees and antagonize M1 receptors in the brain, leading to confusion, memory impairment, and worsening of dementia) - although fesoterodine's active metabolite 5-HMT has limited brain penetration (its quaternary amine metabolite may have reduced CNS entry compared to tolterodine), some CNS effects can still occur. Fesoterodine is contraindicated in patients with urinary retention, gastric retention, uncontrolled narrow-angle glaucoma, and known hypersensitivity to the drug. It should be used with caution in patients with significant bladder outlet obstruction (e.g., benign prostatic hyperplasia, BPH, as urinary retention is a risk), gastrointestinal obstructive disorders (e.g., pyloric stenosis), and in patients with decreased hepatic or renal function (dose adjustment is required; for severe renal impairment (CrCl <30 mL/min) or moderate hepatic impairment, the maximum dose is 4 mg daily). Fesoterodine is also contraindicated during pregnancy and lactation (Category C; risk cannot be ruled out). In preclinical toxicology studies conducted as part of the drug development program, fesoterodine (and its active metabolite 5-HMT) did not show genotoxicity (Ames test, chromosomal aberration assay, micronucleus test) or carcinogenicity (long-term rodent studies at clinically relevant exposure multiples showed no evidence of carcinogenic potential). Reproductive and developmental toxicity studies in rats and rabbits showed no teratogenicity at clinically relevant doses, but embryofetal toxicity was observed at maternally toxic doses. The L-mandelate salt form is not used in the marketed product (the fumarate salt is the clinically approved form for fesoterodine), and therefore no specific toxicology studies for the L-mandelate salt are available; however, since the mandelate counterion is considered a Generally Recognized As Safe (GRAS) substance in pharmaceutical formulations (mandelic acid is a naturally occurring compound used in various products), and since the salt dissociates in the gastrointestinal tract, releasing the pharmacologically active prodrug base and the mandelate ion, the toxicity profile is expected to be equivalent to that of the fumarate salt when the same dose of fesoterodine base is delivered. The mandelate ion itself is of very low toxicity. Fesoterodine L-mandelate is intended for research use only and is not for human consumption as a research chemical, as it is a controlled substance (prescription drug) with potential for adverse effects; it should only be handled by qualified personnel in controlled laboratory settings, with appropriate safety precautions including avoidance of skin contact, eye contact, and inhalation. For in vitro research, the compound should be handled using standard chemical safety practices (gloves, lab coat, eye protection). Any accidental exposure should be treated according to the Material Safety Data Sheet (MSDS). The compound should be stored securely and accounted for. The safety and efficacy for human therapeutic use are established for the fumarate salt formulation marketed as Toviaz; the L-mandelate salt is not intended for human consumption in a research context. For research applications, the compound is typically used at sub-pharmacological or low pharmacological concentrations (nM to low microM range for receptor binding and functional assays; mg/kg range for animal studies).

C₃₄H₄₅NO₆

563.72

563.325

1206695-46-6

Fesoterodine;286930-02-7

44232509

White to off-white solid powder

6.185

3

7

13

41

629

2

CC(C)C(=O)OC1=C(C=C(C=C1)CO)[C@H](CCN(C(C)C)C(C)C)C2=CC=CC=C2.C1=CC=C(C=C1)[C@@H](C(=O)O)O

BUMCIEARGQDQNL-SXTNJFIWSA-N

InChI=1S/C26H37NO3.C8H8O3/c1-18(2)26(29)30-25-13-12-21(17-28)16-24(25)23(22-10-8-7-9-11-22)14-15-27(19(3)4)20(5)6;9-7(8(10)11)6-4-2-1-3-5-6/h7-13,16,18-20,23,28H,14-15,17H2,1-6H3;1-5,7,9H,(H,10,11)/t23-;7-/m10/s1

[2-[(1R)-3-[di(propan-2-yl)amino]-1-phenylpropyl]-4-(hydroxymethyl)phenyl] 2-methylpropanoate;(2S)-2-hydroxy-2-phenylacetic acid

Fesoterodine Lmandelate; Fesoterodine L mandelate

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)

DMSO : ~100 mg/mL (~177.39 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (4.43 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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (4.43 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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (4.43 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 corn oil and mix evenly.

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