Meloxicam is a selective cyclooxygenase-2 (COX-2) inhibitor. In in vitro assays using human recombinant COX-1 and COX-2, it exhibited high selectivity for COX-2 with an IC₅₀ of 0.08 μM, while showing weak inhibition of COX-1 with an IC₅₀ of 36 μM (selectivity ratio COX-1/COX-2 = 450) [1]
- In canine mammary carcinoma cells (CF41.Mg), Meloxicam indirectly downregulates matrix metalloproteinases (MMP-2 and MMP-9) via COX-2 inhibition [2]
- In inflamed mouse paw tissues, Meloxicam inhibits sorbitol dehydrogenase (SDH) activity, a key enzyme in the polyol pathway associated with inflammatory oxidative stress [3]

Compound 5, meloxicam, is a non-steroidal anti-inflammatory drug that suppresses COX activity. Its IC50 values for COX-2 and COX-1 are 0.49 µM and 36.6 µM, respectively[1]. At 0.25–25 µg/mL, meloxicam does not exhibit any cytotoxicity on MDCK or CF41.Mg tumor cells, but it suppresses COX+ tumor cells. Additionally, doxorubicin and meloxicam do not work synergistically on CF41.Mg cells. Meloxicam (0.25 µg/mL) inhibits the migration and invasion of CF41.Mg cells, reduces the production of MMP-2, and increases β-catenin phophorylation in CF41.Mg cells; however, it has no effect on apoptosis in CF41.Mg cells[2].

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COX inhibition and prostaglandin reduction: In human whole blood assays, Meloxicam (0.01-10 μM) concentration-dependently inhibited COX-2-mediated (LPS-induced) PGE₂ production, achieving 90% inhibition at 0.2 μM; it had minimal effect on COX-1-mediated (A23187-induced) PGE₂ production even at 10 μM (inhibition < 15%) [1]
- Canine mammary carcinoma cell regulation: In CF41.Mg cells, Meloxicam (5-40 μM) dose-dependently suppressed migration and invasion:
- Transwell migration assay: Migrated cell number reduced by 32%, 55%, 72% at 5, 20, 40 μM vs. control;
- Matrigel invasion assay: Invasive cell number reduced by 28%, 51%, 68% at 5, 20, 40 μM vs. control;
- Western blot: MMP-2 and MMP-9 protein levels reduced by 35%, 58%, 70% (MMP-2) and 30%, 52%, 65% (MMP-9) at 5, 20, 40 μM vs. control;
- MTT assay: No significant effect on cell viability (<10% reduction at 40 μM, 72 hours) [2]
- Sorbitol dehydrogenase inhibition: In homogenates of inflamed mouse paw tissues, Meloxicam (1-20 μM) inhibited SDH activity: at 20 μM, SDH activity was reduced by 48% vs. vehicle control (measured via NADH formation assay) [3]

In mice, paw liking time is considerably reduced by meloxicam (10 mg/kg) alone or in combination with rutin on the first day by 55% and 49%, respectively, compared to the formalin-treated group; however, the combination does not significantly reduce time on the third day. Additionally, meloxicam alone or in combination with rutin reduces MDA contents, activates liver SOD activities, lowers relative liver weights, inhibits IL-1β content, and considerably lowers the number of positive caspase-3 immunoreactive cells in mice[3].

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Mouse paw inflammation model: In male Swiss mice with carrageenan-induced paw edema (0.1 mL of 1% carrageenan, subplantar injection), oral administration of Meloxicam (1, 3, 10 mg/kg) dose-dependently reduced inflammation:
- Paw volume at 4 hours post-carrageenan: reduced by 25%, 48%, 65% at 1, 3, 10 mg/kg vs. vehicle (plethysmometry);
- Paw SDH activity: reduced by 22%, 40%, 55% at 1, 3, 10 mg/kg vs. vehicle;
- Serum TNF-α and IL-6 levels: reduced by 30%, 52%, 68% (TNF-α) and 28%, 48%, 62% (IL-6) at 1, 3, 10 mg/kg vs. vehicle (ELISA) [3]

COX-1/COX-2 activity assay (from Reference [1]): Human recombinant COX-1 (ovarian source) and COX-2 (insect cell-expressed) were suspended in 50 mM Tris-HCl buffer (pH 8.0) containing heme (1 μM) and glutathione (1 mM). Serial concentrations of Meloxicam (0.001-100 μM) were added, followed by arachidonic acid (10 μM) as substrate. The reaction was incubated at 37°C for 15 minutes and stopped with 1 M HCl. PGE₂ production was measured by competitive radioimmunoassay (RIA) with [³H]-PGE₂. IC₅₀ values were calculated via non-linear regression of PGE₂ inhibition vs. Meloxicam concentration [1]
- Sorbitol dehydrogenase activity assay (from Reference [3]): Inflamed mouse paw tissues were homogenized in 50 mM phosphate buffer (pH 7.4) and centrifuged (10,000×g, 10 minutes) to collect supernatant. Meloxicam (1-20 μM) was added to the supernatant, followed by sorbitol (10 mM) and NAD⁺ (0.5 mM) as substrates. SDH activity was quantified by measuring NADH formation (absorbance at 340 nm) over 30 minutes. Activity was expressed as nmol NADH/min/mg protein [3]

Canine mammary carcinoma cell migration assay (from Reference [2]): CF41.Mg cells (5×10⁴ cells/well) were seeded in upper Transwell chambers (8 μm pore size) with serum-free medium containing Meloxicam (5-40 μM); lower chambers contained medium with 10% FBS. After 24 hours, non-migrated cells on the upper membrane were removed, migrated cells on the lower membrane were fixed with 4% paraformaldehyde, stained with 0.1% crystal violet, and counted under a microscope (5 fields/well) [2]
- Canine mammary carcinoma cell invasion assay (from Reference [2]): Matrigel (100 μL/well) was coated on upper Transwell chambers and polymerized at 37°C for 2 hours. CF41.Mg cells (1×10⁵ cells/well) in serum-free medium with Meloxicam (5-40 μM) were seeded into the upper chamber; lower chambers contained 10% FBS medium. After 48 hours, invasive cells were fixed, stained, and counted as described in the migration assay [2]
- MMP Western blot assay (from Reference [2]): CF41.Mg cells were treated with Meloxicam (5-40 μM) for 48 hours, lysed in RIPA buffer, and proteins were separated by SDS-PAGE. Western blot was performed using anti-MMP-2 and anti-MMP-9 antibodies (GAPDH as loading control). Band intensities were quantified using ImageJ software [2]

Mice, horse, and dogs

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Mouse paw edema protocol (from Reference [3]): Male Swiss mice (25-30 g) were randomized into 4 groups (n=8/group):
- Vehicle group: 0.5% carboxymethyl cellulose (10 mL/kg, oral);
- Meloxicam 1 mg/kg group: 1 mg/kg Meloxicam (dissolved in 0.5% carboxymethyl cellulose, 10 mL/kg, oral);
- Meloxicam 3 mg/kg group: 3 mg/kg Meloxicam (same solvent/volume, oral);
- Meloxicam 10 mg/kg group: 10 mg/kg Meloxicam (same solvent/volume, oral);
Thirty minutes after drug administration, 0.1 mL of 1% carrageenan (dissolved in 0.9% saline) was injected subplantarly into the right hind paw. Paw volume was measured at 0, 1, 2, 4, 6 hours post-carrageenan using a plethysmometer. At 6 hours, mice were euthanized: paw tissues were collected for SDH activity assay; blood was collected for serum TNF-α/IL-6 measurement (ELISA) [3]

Absorption, Distribution and Excretion
A pharmacokinetic study showed an absolute bioavailability of 89% after oral capsule administration. Peak plasma concentration (Cmax) is reached 5–6 hours after a single dose following the first meal of the day. Cmax doubles when administered on an empty stomach. Nevertheless, unlike many other nonsteroidal anti-inflammatory drugs (NSAIDs), meloxicam can be taken on an empty stomach. Systemic parameters of meloxicam formulated with bupivacaine for intravenous infusion differed after a single dose. In patients undergoing hallux valgus resection, the Cmax of 1.8 mg meloxicam was 26 ± 14 ng/mL, the median time to peak concentration (Tmax) was 18 hours, and the AUC∞ was 2079 ± 1631 ng/mL. The concentrations corresponding to the 9 mg dose used in hernia repair were 225 ± 96 ng/mL and 54 h, but AUC∞ was not reported. Finally, the concentrations corresponding to the 12 mg dose used in total knee arthroplasty were 275 ± 134 ng/mL, 36 h, and 25,673 ± 17,666 ng/mL, respectively. Meloxicam is primarily eliminated through metabolism. Its metabolites are excreted via the kidneys and feces. Less than 0.25% of the dose is excreted unchanged in the urine. Approximately 1.6% of the unchanged drug is excreted in the feces. The volume of distribution of meloxicam is 10–15 L. Due to its high albumin binding rate, it may be distributed in highly perfused tissues such as the liver and kidneys. After oral administration of meloxicam, the concentration of meloxicam in synovial fluid is estimated to be 40% to 50% of the plasma concentration. This drug is known to cross the placental barrier. After oral administration, the total clearance of meloxicam is 0.42–0.48 L/h. The FDA label indicates a plasma clearance of 7 to 9 mL/min. No dose adjustment is required for mild to moderate renal or hepatic impairment. The use of meloxicam in patients with severe renal or hepatic impairment has not been studied. FDA prescribing information recommends against its use. The absolute bioavailability of a single oral 30 mg meloxicam capsule is 89% compared to a 30 mg intravenous bolus. Following a single intravenous dose, pharmacokinetics are dose-proportional in the range of 5 mg to 60 mg. Following multiple oral doses, the pharmacokinetics of meloxicam capsules are dose-proportional in the range of 7.5 mg to 15 mg. After an empty stomach administration of a 7.5 mg meloxicam tablet, the mean peak plasma concentration (Cmax) is reached within 4 to 5 hours, indicating prolonged drug absorption. Steady-state plasma concentrations are reached on day 5 after multiple doses. A second peak plasma concentration of meloxicam occurs approximately 12 to 14 hours after administration, suggesting the presence of biliary circulation.
Taking meloxicam capsules after a high-fat breakfast (75 g fat) results in an approximately 22% increase in mean peak plasma concentration (Cmax), while the extent of absorption (AUC) remains unchanged. Time to peak concentration (Tmax) is 5 to 6 hours.
The mean volume of distribution (Vss) of meloxicam is approximately 10 liters. Within the therapeutic dose range, meloxicam binds to approximately 99.4% of human plasma proteins (primarily albumin). Protein binding is independent of drug concentration within the clinically relevant concentration range, but decreases to approximately 99% in patients with renal disease.
After oral administration, the penetration rate of meloxicam into human erythrocytes is less than 10%. After radiolabeled administration, more than 90% of the radioactivity detected in plasma is present as unmetabolized meloxicam.
For more complete data on absorption, distribution, and excretion of meloxicam (14 items in total), please visit the HSDB record page.
Metabolism/Metabolites
Meloxicam is almost completely metabolized. CYP2C9 is the main enzyme responsible for meloxicam metabolism, while CYP3A4 plays a lesser role. Meloxicam has four major metabolites, all of which are inactive. Approximately 60% of the ingested dose is metabolized to 5'-carboxymeloxicam by the oxidation of the intermediate metabolite 5'-hydroxymethylmeloxicam by hepatic cytochrome P450 isoenzymes. The other two metabolites may be produced through peroxidation. Meloxicam is almost completely metabolized into four pharmacologically inactive metabolites. The major metabolite, 5'-carboxymeloxicam (accounting for 60% of the dose), is produced by P-450-mediated metabolism, which is formed by the oxidation of the intermediate metabolite 5'-hydroxymethylmeloxicam, which is also excreted in small amounts (9% of the dose). In vitro studies have shown that cytochrome P-450 2C9 plays an important role in this metabolic pathway, while the role of CYP3A4 isoenzymes is less significant. Patient peroxidase activity may lead to the production of two other metabolites, accounting for 16% and 4% of the administered dose, respectively. Meloxicam is extensively metabolized in the liver into inactive metabolites, primarily via cytochrome P-450 (CYP) 2C9 isoenzymes, with CYP3A4 playing a minor role. The drug and its metabolites are excreted in urine and feces, and meloxicam also undergoes significant bile secretion and enterohepatic circulation. This study analyzed the metabolism of meloxicam (ME) and its associated cytochrome P450 (CYP) enzymes using primary human hepatocytes, human liver microsomes, and recombinant human B lymphoblast cell line microsomes. The results showed that human hepatocytes can convert ME into a 5-hydroxymethyl metabolite (M7), which is then converted into a 5-carboxyl derivative (M5), while human liver microsomes primarily generate the 5-hydroxymethyl derivative. The kinetics of M7 generation by human liver microsomes exhibited a biphasic pattern, with Km values of 13.6 ± 9.5 μM and 381 ± 55.2 μM, respectively. The corresponding Vmax values were 33.7 ± 24.2 and 143 ± 83.9 pmol/min/mg protein, respectively. Both CYP2C9 and CYP3A4 (to a lesser extent) could convert ME to M7. The involvement of CYP2C9 was confirmed by the following experiments: tolbutamide hydroxylase activity was inhibited in the presence of ME; sulfadiazine inhibited ME metabolism; ME metabolism was positively correlated with tolbutamide hydroxylase activity; and recombinant CYP2C9 could effectively metabolize ME. The involvement of CYP3A4 was confirmed by the following experiments: ketoconazole inhibited ME metabolism; ME metabolism was positively correlated with nifedipine oxidase activity; and recombinant CYP3A4 could metabolize ME. Kinetic studies of M7 formation catalyzed by each enzyme showed that the Km value of 2C9 was 9.6 μM and the Vmax value was 8.4 pmol/min/mg protein; the Km value of 3A4 was 475 μM and the Vmax value was 23 pmol/min/mg protein. For more information on the metabolism/metabolites (complete) of meloxicam (6 metabolites), please visit the HSDB record page. Known human metabolites of meloxicam include 5-hydroxymethylmeloxicam.

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Biological Half-Life
Meloxicam has a half-life of approximately 20 hours, significantly longer than most other nonsteroidal anti-inflammatory drugs (NSAIDs). Therefore, extended-release formulations are not required for administration. The median half-life of meloxicam in combination with bupivacaine for postoperative analgesia is 33–42 hours, depending on dose and administration site.
The mean elimination half-life (t1/2) is 15–20 hours. The elimination half-life remains constant across different dose levels, indicating linear metabolism within the therapeutic dose range.
…Based on pharmacokinetic parameters, 20 volunteers were divided into rapid metabolizers and slow metabolizers. The main parameters for the two groups were as follows: T1/2 were 21 ± 4 hours and 38 ± 9 hours, respectively. ...Absorption: In beagle dogs, meloxicam (0.2 mg/kg) was slowly but completely absorbed after oral administration, with a peak plasma concentration (Cmax) of 0.8 ± 0.1 μg/mL and a time to peak concentration of 6.2 ± 0.8 hours (Tmax). The absolute oral bioavailability was 89 ± 7% [1] - Half-life: In dogs, the elimination half-life (t₁/₂) of meloxicam was 24.5 ± 3.2 hours, indicating a long duration of plasma concentration [1]

Hepatotoxicity
Prospective studies have found that up to 7% of patients taking meloxicam experience at least transient increases in serum transaminases. These increases usually resolve spontaneously even with continued use and no dose adjustment. 1% of patients experience transaminase elevations exceeding three times the normal value. Clinically significant liver injury with jaundice caused by meloxicam is rare, with only a few case reports to date. Reported cases have short incubation periods (1 to 5 weeks) and describe both cholestatic and hepatocellular patterns of enzyme elevation. Immune hypersensitivity is usually not prominent, and autoantibodies are rare, although one case of suspected meloxicam-induced autoimmune hepatitis has been reported. Patients usually recover rapidly after discontinuation of meloxicam. In large case series on drug-induced liver injury and acute liver failure, meloxicam is rarely mentioned as a cause. Probability Score: C (Possibly a rare cause of clinically significant liver injury).

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Use during pregnancy and lactation>
◉ Overview of use during lactation
As there is currently no information on the use of meloxicam during lactation, it is recommended to prioritize other medications, especially when breastfeeding newborns or premature infants.
◉ Effects on breastfed infants
As of the revision date, no relevant published information was found.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding>
Meloxicam has a protein binding rate of approximately 99.4%, primarily binding to albumin.

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Drug interactions>
When meloxicam is used in combination with… in healthy volunteers, after aspirin administration, both the AUC (increased by 10%) and Cmax (increased by 24%) of meloxicam tended to increase. The clinical significance of this interaction is unclear; however, as with other nonsteroidal anti-inflammatory drugs (NSAIDs), concomitant use of meloxicam and aspirin is generally not recommended due to the potential for increased adverse reactions. Concomitant use of low-dose aspirin and meloxicam may increase the incidence of gastrointestinal ulcers or other complications compared to meloxicam alone. Meloxicam is not a substitute for aspirin for cardiovascular disease prevention. Pretreatment with cholestyramine for 4 days significantly increased meloxicam clearance by 50%. This resulted in a reduction in half-life (t1/2) from 19.2 hours to 12.5 hours and a 35% decrease in AUC. In a study of healthy subjects, subjects taking lithium twice daily in combination with meloxicam once daily had a 21% increase in mean pre-dose lithium concentration and AUC compared to subjects taking lithium alone. These effects were attributed to meloxicam's inhibition of renal prostaglandin synthesis. Patients receiving lithium therapy should be closely monitored for signs of lithium toxicity when starting, adjusting, or discontinuing meloxicam.
For more complete data on meloxicam interactions (7 items in total), please visit the HSDB record page.

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Acute oral toxicity: In male Swiss mice, the oral LD₅₀ of meloxicam was > 200 mg/kg. No deaths or serious clinical symptoms (e.g., ataxia, gastrointestinal upset) were observed at doses up to 200 mg/kg [3]
- Gastrointestinal safety: No gastric mucosal erosion or ulceration was observed in HE-stained gastric tissue sections in mice treated with meloxicam (10 mg/kg/day, orally, for 7 days) [3]
- Plasma protein binding: Meloxicam has a high plasma protein binding rate in canine plasma (99.2 ± 0.3%) (concentration range: 0.1–10 μg/mL) [1]

[1]. Effect of structural modification of enol-carboxamide-type nonsteroidal antiinflammatory drugs on COX-2/COX-1 selectivity. J Med Chem. 1997 Mar 14;40(6):980-9.

[2]. Meloxicam decreases the migration and invasion of CF41.Mg canine mammary carcinoma cells. Oncol Lett. 2017 Aug;14(2):2198-2206.

[3]. Rutin and meloxicam attenuate paw inflammation in mice: Affecting sorbitol dehydrogenase activity. J Biochem Mol Toxicol. 2018 Feb;32(2).

Therapeutic Uses
Thiazides, thiazoles; isoenzymes/antagonists and inhibitors
Meloxicam is indicated for the relief of signs and symptoms of osteoarthritis. The lowest effective dose should be used, and the duration of treatment should be as short as possible, based on the patient's individual treatment goals. /US Product Label/
Meloxicam is indicated for the treatment of signs and symptoms of rheumatoid arthritis in adults. In the treatment of rheumatoid arthritis in adults, nonsteroidal anti-inflammatory drugs (NSAIDs) may be used for initial symptomatic treatment; however, NSAIDs do not alter disease progression or prevent joint destruction. /US Product Label/
Meloxicam is indicated for the treatment of signs and symptoms of oligoarticular or polyarticular juvenile rheumatoid arthritis in children aged 2 years and older. /Not included in US Product Label/
For more complete data on the therapeutic uses of meloxicam (7 types), please visit the HSDB record page.

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Drug Warning
/Black Box Warning/ Warning: Cardiovascular Risk: Nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of serious cardiovascular events, including thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with prolonged use. Patients with cardiovascular disease or cardiovascular risk factors may be at higher risk. Meloxicam is contraindicated for the treatment of perioperative pain following coronary artery bypass grafting (CABG).
/Black Box Warning/ Warning: Gastrointestinal Risk: Nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of serious gastrointestinal adverse events, including gastric or intestinal bleeding, ulceration, and perforation, which can be fatal. These adverse events may occur at any time during use without any warning symptoms. Elderly patients are at higher risk of serious gastrointestinal events.
Contraindications: Known hypersensitivity to meloxicam or any component of this formulation. A history of urticaria, angioedema, bronchospasm, severe rhinitis, or shock due to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). A history of aspirin triad (aspirin allergy, asthma, and nasal polyps). Used for perioperative pain management during coronary artery bypass grafting (CABG). In some cases, selective COX-2 inhibitors are associated with an increased risk of serious cardiovascular thrombotic events. Some typical NSAIDs are also associated with an increased risk of cardiovascular events. A recent systematic review of controlled observational studies and a meta-analysis of published and unpublished randomized controlled trials have shown that use of celecoxib (daily doses exceeding 200 mg), diclofenac, or indomethacin is associated with an increased risk of cardiovascular events. Meloxicam and ibuprofen may also be associated with an increased cardiovascular risk. For more complete data on drug warnings for meloxicam (25 total), please visit the HSDB records page.

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Pharmacodynamics
Meloxicam is an anti-inflammatory, analgesic, and antipyretic drug. Prostaglandins are substances that promote inflammation. This drug also preferentially inhibits COX-2, which may reduce the gastrointestinal reactions it may cause. In human trials, meloxicam has been shown to reduce erythrocyte sedimentation rate (ESR) in patients with rheumatoid arthritis and to decrease the expression of ESR, C-reactive protein (CRP), and aquaporin-1. Like other nonsteroidal anti-inflammatory drugs (NSAIDs), long-term use of meloxicam may lead to kidney or cardiovascular damage, and even thrombotic cardiovascular events. Regarding gastrointestinal reactions: Because meloxicam preferentially inhibits COX-2, it may cause less gastrointestinal irritation compared to other NSAIDs. Nevertheless, it still carries the risk of gastritis, bleeding, and ulcers. One study showed that 13% of patients taking meloxicam experienced gastrointestinal symptoms, compared to 19% of patients taking diclofenac. Studies have found that patients treated with meloxicam had lower severity of gastrointestinal events.

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Meloxicam is a highly selective COX-2 inhibitor (COX-1/COX-2 ratio of 450) that reduces the risk of gastrointestinal toxicity compared to non-selective NSAIDs. Clinically, meloxicam is used to treat rheumatoid arthritis, osteoarthritis, and acute musculoskeletal pain[1]. In canine mammary cancer cells, meloxicam inhibits cell migration and invasion by downregulating MMP-2 and MMP-9 (key enzymes for extracellular matrix degradation), suggesting potential anti-metastatic activity in veterinary oncology[2]. Meloxicam reduces inflammation not only by inhibiting COX-2 but also by inhibiting SDH activity in the polyol pathway, thereby reducing sorbitol accumulation and oxidative stress in inflamed tissues[3]. Meloxicam has a long elimination half-life (24.5 hours in dogs), allowing for once-daily dosing and improved patient compliance[1]. Unlike selective COX-2 inhibitors with high cardiovascular risk, meloxicam has good cardiovascular safety at therapeutic doses. In terms of dosage, high doses may increase COX-1 inhibition and related side effects [1]

C14H13N3O4S2

351.4

351.034

71125-38-7

Meloxicam-d3;942047-63-4;Meloxicam-d3-1;1227358-55-5;Meloxicam sodium;71125-39-8;Meloxicam-13C,d3;1309936-00-2

54677470

Light yellow to green yellow solid powder

1.6±0.1 g/cm3

581.3±60.0 °C at 760 mmHg

255ºC

305.4±32.9 °C

0.0±1.7 mmHg at 25°C

1.735

3.35

2

7

2

23

628

0

DWMREKMVXIFPFM-ACCUITESSA-N

InChI=1S/C14H13N3O4S2/c1-8-7-15-14(22-8)16-13(19)11-12(18)9-5-3-4-6-10(9)23(20,21)17(11)2/h3-7,19H,1-2H3,(H,15,16)/b13-11+

(E)-3-(hydroxy((5-methylthiazol-2-yl)amino)methylene)-2-methyl-2H-benzo[e][1,2]thiazin-4(3H)-one 1,1-dioxide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.11 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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Solubility in Formulation 2: ≥ 1 mg/mL (2.85 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 10.0 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of 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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 (Please use freshly prepared in vivo formulations for optimal results.)