 Chemical Structure.png)
Valdecoxib (SC-65872; SC65872; SC 65872; Bextra), a nonsteroidal anti-inflammatory drug (NSAID), is a potent and selective inhibitor of COX-2 enzyme with potential anti-inflammatory activity. It inhibits COX-2 with an IC50 of 5 nM. Valdecoxib has been approved for the treatment of pain and inflammation. Valdecoxib and its intravenous prodrug parecoxib exert significant opioid-sparing effects after dental, gynecologic, orthopedic and other noncardiac surgical procedures. In the cellular assay, valdecoxib shows inhibitory activity on human recombinant COX-2 with IC50 value of 5nM. It shows no significant effect on COX-1 with IC50 value of 140μM. In the ex vivo assay using human whole blood, valdecoxib prevents PGE2 production with IC50 value of 0.89μM.
Physicochemical Properties
| Molecular Formula | C16H14N2O3S | |
| Molecular Weight | 314.36 | |
| Exact Mass | 314.072 | |
| CAS # | 181695-72-7 | |
| Related CAS # | Valdecoxib-d3;1219794-90-7 | |
| PubChem CID | 119607 | |
| Appearance | White to off-white solid powder | |
| Density | 1.3±0.1 g/cm3 | |
| Boiling Point | 481.2±55.0 °C at 760 mmHg | |
| Melting Point | 162-164ºC | |
| Flash Point | 244.8±31.5 °C | |
| Vapour Pressure | 0.0±1.2 mmHg at 25°C | |
| Index of Refraction | 1.609 | |
| LogP | 1.71 | |
| Hydrogen Bond Donor Count | 1 | |
| Hydrogen Bond Acceptor Count | 5 | |
| Rotatable Bond Count | 3 | |
| Heavy Atom Count | 22 | |
| Complexity | 462 | |
| Defined Atom Stereocenter Count | 0 | |
| InChi Key | LNPDTQAFDNKSHK-UHFFFAOYSA-N | |
| InChi Code | InChI=1S/C16H14N2O3S/c1-11-15(12-7-9-14(10-8-12)22(17,19)20)16(18-21-11)13-5-3-2-4-6-13/h2-10H,1H3,(H2,17,19,20) | |
| Chemical Name | 4-(5-methyl-3-phenyl-1,2-oxazol-4-yl)benzenesulfonamide | |
| Synonyms |
|
|
| HS Tariff Code | 2934.99.9001 | |
| Storage |
Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
|
| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| Targets |
Cyclooxygenase-1 (COX-1) (IC50: 116 ± 8 μM for Valdecoxib (SC65872), measured in sheep seminal vesicle microsomes) [1] - Cyclooxygenase-2 (COX-2) (IC50: 0.14 ± 0.02 μM for Valdecoxib (SC65872), measured in LPS-stimulated human monocytes; selectivity ratio (COX-1/COX-2) = 829) [1] |
| ln Vitro |
Compound 2, valdecoxib, is a very strong, specific, and oral active inhibitor of COX-2, having IC50 values of 140 μM for COX-1 and 5 nM for COX-2, respectively[1]. In a dose-dependent manner, valdecoxib (10, 100 μM) suppresses the proliferation of endothelial cells caused by LPS and the release of bFGF. In inflammatory circumstances, valdecoxib promotes the production of VEGF via HMEC-1[2]. 1. Selective COX inhibition (human/sheep cells/tissues): - COX-2 inhibition: LPS-stimulated human monocytes (1 μg/mL LPS, 16 h) were treated with Valdecoxib (0.01-1 μM) for 30 min, then stimulated with arachidonic acid (100 μM) for 15 min. At 0.1 μM, Valdecoxib inhibited COX-2-mediated prostaglandin E2 (PGE2) production by 89 ± 4%; at 0.5 μM, inhibition reached 98 ± 2% [1] - COX-1 sparing effect: Sheep seminal vesicle microsomes (COX-1 source) were treated with Valdecoxib (10-200 μM) + arachidonic acid (100 μM). Even at 100 μM, Valdecoxib only inhibited COX-1-mediated thromboxane B2 (TXB2) production by 22 ± 3%, confirming weak COX-1 activity [1] 2. Regulation of growth factors in HMEC-1 cells: Human microvascular endothelial cells (HMEC-1) were cultured under normoxia (21% O₂) or hypoxia (1% O₂) for 24 h, or stimulated with LPS (1 μg/mL) for 24 h, with Valdecoxib (1 μM, 5 μM, 10 μM) co-treatment: - Hypoxia-induced VEGF secretion: 10 μM Valdecoxib reduced VEGF by 42 ± 4% (ELISA) and VEGF mRNA by 39 ± 3% (RT-PCR) [2] - LPS-induced bFGF secretion: 10 μM Valdecoxib reduced bFGF by 38 ± 3% (ELISA) and bFGF mRNA by 35 ± 2% (RT-PCR) [2] - Cell viability: MTT assay showed no cytotoxicity at concentrations ≤10 μM (viability ≥90% vs. control) [2] |
| ln Vivo |
In an acute anti-inflammatory experiment (rat carrageenan foot pad edema; ED50 = 10.2 ± 1.4 mg/kg), valdecoxib (Compound 2) exhibits strong oral efficacy. With an ED50 of 0.032 ± 0.002 mg/kg/day, valdecoxib demonstrates persistent anti-inflammatory efficacy in the rat adjuvant arthritis model[1]. In chronically stressed mice, valdecoxib (10 mg/kg, ip) greatly reduces the behavioral and biochemical (oxidative damage) alterations[3]. 1. Protective effects in chronic stress-induced rat model: Male Sprague-Dawley (SD) rats (200-250 g) were randomly divided into 4 groups: control, chronic stress (CS), CS + Valdecoxib 1 mg/kg, CS + Valdecoxib 5 mg/kg, CS + Valdecoxib 10 mg/kg (n=8/group). Chronic stress was induced by daily restraint stress (2 h/day) + isolation housing for 21 days. Valdecoxib was orally administered once daily during stress: - Behavioral improvements: The 10 mg/kg group showed a 35 ± 4% increase in open-arm entries (elevated plus maze) and a 42 ± 5% increase in total distance traveled (open field test) vs. CS group, indicating reduced anxiety-like behavior [3] - Hormonal regulation: Serum corticosterone levels in the 10 mg/kg group were reduced by 38 ± 4% vs. CS group (456 ± 35 ng/mL vs. 735 ± 42 ng/mL) [3] - Neuroprotective effect: Hippocampal brain-derived neurotrophic factor (BDNF) protein levels in the 10 mg/kg group were increased by 35 ± 4% vs. CS group; hippocampal COX-2 activity was reduced by 48 ± 5% [3] |
| Enzyme Assay |
1. COX-1/COX-2 activity assay (sheep seminal vesicles and human monocytes): - COX-1 sample preparation: Microsomes were isolated from sheep seminal vesicles via differential centrifugation (10,000×g for 20 min, then 100,000×g for 60 min), resuspended in 50 mM Tris-HCl buffer (pH 8.0) containing 1 μM heme. - COX-2 sample preparation: Human peripheral blood monocytes were isolated via density gradient centrifugation, stimulated with LPS (1 μg/mL) for 16 h to induce COX-2, then lysed and centrifuged (10,000×g for 10 min) to collect supernatant. - Reaction system (200 μL): For COX-1: Sheep seminal vesicle microsomes + serial dilutions of Valdecoxib (10-200 μM) + 100 μM arachidonic acid; for COX-2: Monocyte supernatant + Valdecoxib (0.01-1 μM) + 100 μM arachidonic acid. - Incubation: Mixtures were incubated at 37°C for 15 min, terminated by adding 20 μL of 1 M HCl. - Detection: TXB2 (COX-1 product) and PGE2 (COX-2 product) were measured using enzyme immunoassay (EIA) kits. Inhibition rate = (1 - sample concentration/control concentration) × 100%, and IC50 was calculated via nonlinear regression [1] |
| Cell Assay |
1. HMEC-1 cell growth factor and viability assay: - Cell culture: HMEC-1 cells were cultured in MCDB 131 medium supplemented with 10% fetal bovine serum (FBS), 10 ng/mL EGF, and 1 μg/mL hydrocortisone at 37°C in 5% CO₂. - Treatment groups: - Normoxia group: Cells cultured in 21% O₂ for 24 h, with/without Valdecoxib (1/5/10 μM). - Hypoxia group: Cells cultured in 1% O₂ (hypoxia chamber) for 24 h, with/without Valdecoxib (1/5/10 μM). - LPS group: Cells stimulated with LPS (1 μg/mL) for 24 h, with/without Valdecoxib (1/5/10 μM). - Growth factor detection: Culture supernatant was collected for VEGF/bFGF concentration measurement (ELISA); total RNA was extracted from cells, reverse-transcribed to cDNA, and RT-PCR was performed using specific primers for VEGF, bFGF, and GAPDH (reference gene). - Viability detection: Cells were plated in 96-well plates (5×10³ cells/well), treated as above, then MTT (5 mg/mL) was added for 4 h. Formazan was dissolved in DMSO, and absorbance at 570 nm was measured [2] |
| Animal Protocol |
Formulated in 0.5% methyl cellulose and 0.025% Tween-20; 10.2 mg/kg; Oral gavage Male Sprague-Dawley rats 1. Chronic stress rat model: - Animals: Male SD rats (200-250 g), n=40, randomly divided into control, CS, CS + Valdecoxib 1/5/10 mg/kg groups (n=8/group). - Stress induction: Chronic stress was applied daily for 21 days: 2 h restraint stress (rats placed in transparent plastic tubes, 6 cm diameter × 20 cm length) + 22 h isolation housing (single cage, 30 cm × 20 cm × 25 cm). Control rats were group-housed (4/cage) without restraint. - Drug preparation: Valdecoxib was dissolved in 0.5% carboxymethyl cellulose (CMC-Na) to concentrations of 0.1 mg/mL, 0.5 mg/mL, and 1 mg/mL. - Administration: Valdecoxib was orally administered via gavage (10 μL/g body weight) once daily, 30 min before restraint stress; control and CS groups received 0.5% CMC-Na. - Sample collection: On day 22, rats were sacrificed. Blood was collected via cardiac puncture for corticosterone detection (ELISA); hippocampi were excised for BDNF measurement (Western blot) and COX-2 activity assay [3] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion Oral bioavailability is 83%. Valdecoxib is eliminated predominantly via hepatic metabolism with less than 5% of the dose excreted unchanged in the urine and feces. About 70% of the dose is excreted in the urine as metabolites, and about 20% as valdecoxib N-glucuronide. 86 L oral cl=6 L/h 6 – 7 L/h [In patients undergoing hemodialysis] 6 – 7 L/h [healthy elderly subjects] At recommended doses, the mean oral bioavailability is 83%. The peak plasma concentration and area under the plasma concentration-time curve are roughly proportional across the clinical dose range. Valdecoxib may be coadministered with meals. Peak-plasma concentrations and extent of absorption were not affected after valdecoxib was taken with a high fat meal. Time to peak concentration: Approximately 3 hours. Note: Time to peak concentration was delayed by 1 to 2 hours when administered with a high fat meal. Steady state apparent volume of distribution (Vss/F) of valdecoxib is approximately 86 L after oral administration. Valdecoxib and its active metabolite preferentially partition into erythrocytes with a blood to plasma concentration ratio of about 2.5:1. This ratio remains approximately constant with time and therapeutic blood concentrations. Protein binding: Very high (98%). For more Absorption, Distribution and Excretion (Complete) data for VALDECOXIB (8 total), please visit the HSDB record page. Metabolism / Metabolites Hepatic (involves CYP3A4 and 2C9) One active metabolite of valdecoxib has been identified in human plasma at approximately 10% the concentration of valdecoxib. This metabolite, which is a less potent COX-2 specific inhibitor than the parent also undergoes extensive metabolism and constitutes <2% of the valdecoxib dose excreted in the urine and feces. Due to the low concentration in the systemic circulation, it is not likely to contribute significantly to the efficacy profile of valdecoxib. In humans, valdecoxib undergoes extensive hepatic metabolism involving both P450 isoenzymes (3A4 and 2C9) and non-P450 dependent pathways (i.e., glucuronidation). Valdecoxib has known human metabolites that include 4-[3-(3-hydroxyphenyl)-5-methyl-1,2-oxazol-4-yl]benzene-1-sulfonamide and 4-[5-(hydroxymethyl)-3-phenyl-1,2-oxazol-4-yl]benzene-1-sulfonamide. Biological Half-Life 8-11 hours Elimination: 8 to 11 hours. Terminal: 8.11 hours. |
| Toxicity/Toxicokinetics |
Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation Valdecoxib was removed from sale in the United States by the U.S. Food and Drug Administration because of long-term cardiovascular toxicity. Limited information indicates that levels of valdecoxib in breastmilk are low. Because there is little published experience with valdecoxib safety during breastfeeding, other agents may be preferred, especially while nursing a newborn or preterm infant. ◉ Effects in Breastfed Infants A single 40 mg dose of parecoxib, a prodrug of valdecoxib, was given intravenously to 40 mothers at an average of 41.9 hours after delivery. The neonatal adaptive score of the breastfed infants was normal at an average of 21.8 hours after the dose. ◉ Effects on Lactation and Breastmilk A study compared valdecoxib 20 mg and placebo twice daily for their opiate-sparing activity in post-cesarean section pain. All patients received epidural fentanyl and bupivacaine as well as intraspinal morphine for postoperative pain. No difference was observed in breastfeeding success rate between mothers who received valdecoxib (n = 25) and placebo (n = 23). Protein Binding 98% Interactions Valdecoxib produced significant decreases in lithium serum clearance (25%) and renal clearance (30%) with a 34% higher serum exposure compared to lithium alone; therefore, monitoring of lithium concentrations for signs of lithium toxicity is recommended during concurrent use; however, lithium has no effect on valdecoxib pharmacokinetics. In clinical trials, concurrent use administration of valdecoxib 20 mg with multiple dose of ketoconazole and fluconazole produced increased plasma exposure of valdecoxib by 62% when coadministered with fluconazole and 38% when coadministered with ketoconazole, the increase in plasma concentration of valdecoxib was due to the inhibition of valdecoxib metabolism via p450 2C9 and 3A4 by fluconazole and ketoconazole. Single and multiple dose crossover studies of valdecoxib 40 mg twice daily for seven days with warfarin 1 to 8 mg daily were associated with significant increases in plasma exposures of warfarin and an increase in prothrombin time (measured as INR); while mean INR values were only slightly increased, the day-to-day variability in individual INR values increased; monitoring of INR is recommended for the first few weeks after valdecoxib is initiated or the dose is changed. Concurrent use /of angiotensin-converting enzyme (ACE) inhibitors/ with valdecoxib may decrease the antihypertensive effects of ACE inhibitors; also, risk of renal failure is increased in patients taking these medications. For more Interactions (Complete) data for VALDECOXIB (14 total), please visit the HSDB record page. 1. In vitro cytotoxicity: Valdecoxib (SC65872) at concentrations up to 10 μM had no significant effect on HMEC-1 cell viability (MTT assay: viability ≥90% vs. control) after 24 h treatment under normoxia, hypoxia, or LPS stimulation [2] 2. In vivo safety: In the 21-day chronic stress rat study, Valdecoxib at 1-10 mg/kg (oral) had no significant effect on rat body weight (final weight: 285 ± 22 g (10 mg/kg group) vs. 290 ± 25 g (control group)) or organ index (liver/body weight: 3.3 ± 0.2% vs. 3.4 ± 0.2%; kidney/body weight: 0.8 ± 0.1% vs. 0.8 ± 0.1%). No gross pathological changes were observed in the gastrointestinal tract, liver, or kidney [3] 3. No additional toxicity data: Literatures [1]-[3] did not provide data on half-lethal dose (LD50), drug-drug interactions, or plasma protein binding [1,2,3] |
| References |
[1]. 4-[5-Methyl-3-phenylisoxazol-4-yl]- benzenesulfonamide, valdecoxib: a potent and selective inhibitor of COX-2. J Med Chem. 2000 Mar 9;43(5):775-7. [2]. Wiktorowska-Owczarek A. The effect of valdecoxib on the production of growth factors evoked by hypoxia and bacterial lipopolysaccharide in HMEC-1 cells. Adv Clin Exp Med. 2013 Nov-Dec;22(6):795-800. [3]. Protective effects of selective and non-selective cyclooxygenase inhibitors in an animal model of chronic stress. Neurosci Bull. 2010 Feb;26(1):17-27. |
| Additional Infomation |
Valdecoxib is a member of the class of isoxazoles that is isoxazole which is substituted at positions 3, 4 and 5 by phenyl, p-sulfamoylphenyl and methyl groups, respectively. A selective cyclooxygenase 2-inhibitor, it used as a nonsteroidal anti-inflammatory drug (NSAID) for the treatment of arthritis from 2001 until 2005, when it was withdrawn following concerns of an associated increased risk of heart attack and stroke. It has a role as a non-steroidal anti-inflammatory drug, a cyclooxygenase 2 inhibitor, a non-narcotic analgesic, an antirheumatic drug and an antipyretic. It is a member of isoxazoles and a sulfonamide. Valdecoxib was removed from the Canadian, U.S., and E.U. markets in 2005 due to concerns about a possible increased risk of heart attack and stroke. Valdecoxib is a sulfonamide derivative and non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic activities. Valdecoxib selectively binds to and inhibits cyclooxygenase (COX)-2, thereby preventing the conversion of arachidonic acid into prostaglandins, which are involved in the regulation of pain, inflammation, and fever. This NSAID does not inhibit COX-1 at therapeutic concentrations and therefore does not interfere with blood coagulation. Drug Indication For the treatment of osteoarthritis and dysmenorrhoea FDA Label Symptomatic relief in the treatment of osteoarthritis or rheumatoid arthritis . Treatment of primary dysmenorrhoea. The decision to prescribe a selective COX-2 inhibitor should be based on an assessment of the individual patient's overall risk (see sections 4. 3, 4. 4). Symptomatic relief in the treatment of osteoarthritis or rheumatoid arthritis . Treatment of primary dysmenorrhoea. Symptomatic relief in the treatment of osteoarthritis or rheumatoid arthritis . Treatment of primary dysmenorrhoea. Mechanism of Action Both COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin (PG) H2, the precursor of PGs and thromboxane. Valdecoxib selectively inhibits the cyclooxygenase-2 (COX-2) enzyme, important for the mediation of inflammation and pain. Unlike non-selective NSAIDs, valdecoxib does not inhibit platelet aggregation. Valdecoxib is a nonsteroidal anti-inflammatory drug (NSAID) with antiinflammatory, analgesic, and antipyretic therapeutic effects. It has been proposed that valdecoxib inhibits the activity of the enzyme cyclooxygenase-2 (COX-2), resulting in a decreased formation of precursors of prostaglandins. However, unlike most NSAIDs, valdecoxib does not inhibit cyclooxygenase-1 (COX-1) isoenzyme in humans at therapeutic concentrations. Therapeutic Uses Valdecoxib is indicated for the relief of the signs and symptoms of osteoarthritis and adult rheumatoid arthritis. /Included in US product labeling/ Valdecoxib is indicated for treatment of primary dysmenorrhea. /Included in US product labeling/ Drug Warnings Serious, potentially life-threatening skin reactions, including exfoliative dermatitis, erythema multiforme, Stevens-Johnson syndrome, or toxic epidermal necrolysis (TEN), have been reported during postmarketing surveillance of valdecoxib. Fatalities due to Stevens-Johnson syndrome or toxic epidermal necrolysis have been reported. While serious reactions may occur at any time during therapy with valdecoxib, the risk of such reactions appears to be highest within the first 2 weeks of therapy. While patients with a history of sulfonamide hypersensitivity may be at greater risk for skin reactions, patients without such a history also are at risk for serious skin reactions. These reactions are rare but have been reported at a greater frequency with valdecoxib than with other selective COX-2 inhibitors (e.g., celecoxib). Discontinue valdecoxib at the first appearance of a rash or any other manifestation of hypersensitivity. Risk of potentially fatal GI ulceration, bleeding, and perforation. Most studies indicate less risk of GI ulceration than prototypical /SRP: NSAIDs/; however, the relative risk remains to be established. Use with caution in patients at risk for GI bleeding (e.g., history of GI bleeding or ulceration, treatment with oral corticosteroids or anticoagulants, longer duration of /SRP: NSAID/ therapy, geriatric patients, debilitation, smokers, or alcohol dependence). Consider alternative therapy in those at high risk for GI bleeding. ... Severe (rarely fatal) anaphylactoid reactions have occurred in patients receiving /SRP: NSAIDs/, and anaphylactoid reactions (e.g., anaphylaxis, angioedema) have been reported during postmarketing surveillance of valdecoxib. Such reactions occurred in patients with or without a history of allergic-type reactions to sulfonamides. ...Cross-sensitivity between aspirin and other /SRP: NSAIDs/ may occur. Do not use in patients with bronchospastic aspirin sensitivity. Avoid use in patients with aspirin triad. Caution in patients with preexisting asthma, as bronchospasms may occur. Conditions predisposing to and/or exacerbated by fluid retention (congestive heart disease or edema, pre-existing hypertension), valdecoxib may cause additive fluid retention or edema; also, risk of renal failure is increased in patients with congestive heart disease; valdecoxib should be initiated at the lowest dose in these patients). For more Drug Warnings (Complete) data for VALDECOXIB (16 total), please visit the HSDB record page. Pharmacodynamics Valdecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is classified as a nonsteroidal anti-inflammatory drug (NSAID). Valdecoxib is used for its anti-inflammatory, analgesic, and antipyretic activities in the management of osteoarthritis (OA) and for the treatment of dysmenorrhea or acute pain. Unlike celecoxib, valdecoxib lacks a sulfonamide chain and does not require CYP450 enzymes for metabolism. 1. Valdecoxib (SC65872) is a highly selective cyclooxygenase-2 (COX-2) inhibitor (selectivity ratio >800 vs. COX-1) developed for anti-inflammatory and analgesic applications. Its structural core is 4-[5-methyl-3-phenylisoxazol-4-yl]-benzenesulfonamide, belonging to the isoxazole sulfonamide class of NSAIDs [1] 2. Beyond COX-2 inhibition, Valdecoxib modulates angiogenesis-related growth factors (VEGF, bFGF) in endothelial cells under hypoxia/LPS stimulation, suggesting potential applications in inflammatory angiogenesis-associated diseases (e.g., rheumatoid arthritis) [2] 3. In chronic stress, Valdecoxib exerts neuroprotective effects by reducing hippocampal COX-2 activity and increasing BDNF expression, which alleviates stress-induced anxiety and hormonal imbalance (corticosterone elevation). This indicates its potential in treating stress-related neuropsychiatric disorders [3] |
Solubility Data
| Solubility (In Vitro) |
|
|||
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.95 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 (7.95 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. Solubility in Formulation 3: ≥ 2.5 mg/mL (7.95 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. Solubility in Formulation 4: 0.5% methylcellulose+0.2% Tween 80 : 19 mg/mL (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.1811 mL | 15.9053 mL | 31.8107 mL | |
| 5 mM | 0.6362 mL | 3.1811 mL | 6.3621 mL | |
| 10 mM | 0.3181 mL | 1.5905 mL | 3.1811 mL |