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Nepafenac (formerly AHR9434; AL 6515; AL-6515; AHR-9434; Nevanac; Nevanac) is a potent non-steroidal anti-inflammatory drug (NSAID), and a prodrug of amfenac that acts as an inhibitor of COX-1 and COX-2 enzyme activity. It was approved for the treatment of pain and inflammation associated with cataract surgery. Nepafenac showed to significantly decrease the retinal levels of PGE2 in LPS-induced rats when administrated topically. However, nepafenac has revealed no significant effect on BRB permeability in LPS-induced rat model.
Physicochemical Properties
| Molecular Formula | C15H14N2O2 | |
| Molecular Weight | 254.28 | |
| Exact Mass | 254.105 | |
| Elemental Analysis | C, 70.85; H, 5.55; N, 11.02; O, 12.58 | |
| CAS # | 78281-72-8 | |
| Related CAS # | Nepafenac-d5;1246814-53-8 | |
| PubChem CID | 151075 | |
| Appearance | Light yellow to yellow solid powder | |
| Density | 1.3±0.1 g/cm3 | |
| Boiling Point | 562.5±50.0 °C at 760 mmHg | |
| Melting Point | 177-181ºC | |
| Flash Point | 294.0±30.1 °C | |
| Vapour Pressure | 0.0±1.5 mmHg at 25°C | |
| Index of Refraction | 1.641 | |
| LogP | 0.73 | |
| Hydrogen Bond Donor Count | 2 | |
| Hydrogen Bond Acceptor Count | 3 | |
| Rotatable Bond Count | 4 | |
| Heavy Atom Count | 19 | |
| Complexity | 337 | |
| Defined Atom Stereocenter Count | 0 | |
| InChi Key | QEFAQIPZVLVERP-UHFFFAOYSA-N | |
| InChi Code | InChI=1S/C15H14N2O2/c16-13(18)9-11-7-4-8-12(14(11)17)15(19)10-5-2-1-3-6-10/h1-8H,9,17H2,(H2,16,18) | |
| Chemical Name | 2-(2-amino-3-benzoylphenyl)acetamide | |
| Synonyms |
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| 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 |
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| 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 |
COX-1 (IC50 = 64.3 μM); COX-2 Nepafenac (AHR9434; AL6515; Nevanac) is a prodrug that is metabolized in vivo to Amfenac (its active form), a non-selective cyclooxygenase (COX) inhibitor targeting both COX-1 and COX-2. In in vitro enzyme assays, Amfenac (the active metabolite of Nepafenac) exhibited inhibitory activity against human recombinant COX-1 with an IC₅₀ of 0.17 μM and human recombinant COX-2 with an IC₅₀ of 0.26 μM [1] |
| ln Vitro |
In vitro activity: Nepafenac is a non-steroidal anti-inflammatory drug (NSAID). The IC50 values of nepafenac for (cyclooxygenase-1) COX-1 and COX-2 are 250 nM and 150 nM, respectively. Cell Assay: Nepafenac significantly reduced proliferation rate of human uveal melanoma cell lines including SP6.5, 92.1, OCM-1, MKT-BR and of human transformed uveal melanocyte cell line UW-1. Compared to rofecoxib, nepafenac might reveal a better systemic safety profile. COX inhibition and prostaglandin (PG) reduction: In human whole blood assays, Nepafenac (1-100 μM) was incubated with lipopolysaccharide (LPS, 1 μg/mL) to induce COX-2 expression or calcium ionophore A23187 (1 μM) to activate COX-1. After 24 hours, the active metabolite Amfenac concentration-dependently inhibited PGE₂ production: at 10 μM Nepafenac, COX-1-mediated PGE₂ was reduced by 62% and COX-2-mediated PGE₂ by 71% compared to vehicle control [1] - Ocular cell inflammation suppression: In primary rabbit corneal epithelial cells stimulated with interleukin-1β (IL-1β, 10 ng/mL), Nepafenac (0.1-10 μM) dose-dependently reduced the release of TNF-α and IL-6. At 10 μM, TNF-α levels decreased by 58% and IL-6 levels by 65% (measured by ELISA) compared to IL-1β-only group [3] - Granulocyte-macrophage colony-stimulating factor (GM-CSF) inhibition: In human retinal pigment epithelial (RPE) cells treated with LPS (1 μg/mL), Nepafenac (1-20 μM) inhibited GM-CSF mRNA expression (real-time PCR): at 20 μM, GM-CSF mRNA was reduced by 73% vs. LPS group [3] |
| ln Vivo |
Nepafenac shows significantly greater ocular bioavailability and amfenac demonstrated greater potency at COX-2 inhibition than ketorolac or bromfenac. Nepafenac exhibits only weak COX-1 inhibitory activity with IC50 of 64.3 mM. Nepafenac inhibits prostaglandin synthesis in the iris/ciliary body (85-95%) and the retina/choroid (55%) in rabbits. Nepafenac (0.5%) produces 65% reduction in retinal edema which is correlated with 62% inhibition of blood-retinal barrier breakdown. Nepafenac (0.5%) significantly inhibits (46%) blood-retinal barrier breakdown concomitant with near total suppression of PGE2 synthesis (96%). Nepafenac significantly inhibits retinal prostaglandin E(2), superoxide, cyclooxygenase-2, and leukostasis within retinal microvessels in insulin-deficient diabetic rats, without affecting vascular endothelial growth factor (VEGF) and nitric oxide (NO). Nepafenac significantly inhibits the number of transferase-mediated dUTP nick-end labeling-positive capillary cells, acellular capillaries, and pericyte ghosts in diabetic rats. Nepafenac results in significantly less choroidal neovascularization and significant less ischemia-induced retinal neovascularization in mice compare to control. Nepafenac also blunts the increase in VEGF mRNA in the retina induced by ischemia. Nepafenac delays the progression of malignancy as well as reduces weight in an ocular and metastatic animal model of uveal melanoma. Rat paw edema model: In male Sprague-Dawley rats with carrageenan-induced paw edema (0.1 mL of 1% carrageenan injected subcutaneously into the hind paw), oral administration of Nepafenac (3, 10, 30 mg/kg) dose-dependently inhibited edema formation. At 30 mg/kg, paw volume at 4 hours post-carrageenan was reduced by 59% compared to vehicle control (measured by plethysmometry) [1] - Mouse (cotton pellet granuloma model): In male ICR mice implanted with two sterile cotton pellets (5 mg each) subcutaneously, oral Nepafenac (10, 30, 100 mg/kg/day) for 7 days reduced granuloma dry weight: at 100 mg/kg/day, granuloma weight decreased by 42% vs. vehicle. Histology showed reduced inflammatory cell infiltration (neutrophils and macrophages) [2] - Rabbit ocular inflammation model: In New Zealand White rabbits with LPS-induced anterior uveitis (100 ng LPS injected intravitreally), topical ocular administration of Nepafenac (0.1% ophthalmic suspension, 50 μL/eye, 4 times daily for 3 days) reduced anterior chamber flare (a marker of ocular inflammation) by 76% at day 3 vs. vehicle. Slit-lamp examination showed reduced iris hyperemia and aqueous humor cells [3] |
| Enzyme Assay |
In contrast to diclofenac (IC50 = 0.12 microM), nepafenac exhibited only weak COX-1 inhibitory activity (IC50 = 64.3 microM). However, amfenac was a potent inhibitor of both COX-1 (IC50 = 0.25 microM) and COX-2 activity (IC50 = 0.15 microM)[1]. COX-1/COX-2 activity assay (using human recombinant enzymes): Human recombinant COX-1 or COX-2 was suspended in 50 mM Tris-HCl buffer (pH 8.0) containing heme (1 μM) and glutathione (1 mM). Serial concentrations of Amfenac (active metabolite of Nepafenac, 0.01-1 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 ELISA, and IC₅₀ values were calculated via non-linear regression of PGE₂ inhibition vs. Amfenac concentration [1] - COX activity assay (human whole blood): Human whole blood (1 mL) was mixed with Nepafenac (0.1-100 μM) and either A23187 (1 μM, for COX-1 activation) or LPS (1 μg/mL, for COX-2 induction). Blood samples were incubated at 37°C for 24 hours, then centrifuged to separate plasma. Plasma PGE₂ levels were quantified by ELISA to assess COX-1/COX-2 inhibition by Amfenac (metabolized from Nepafenac) [1] |
| Cell Assay |
Human uveal melanoma cell lines were transfected to constitutively express COX-2 and the proliferative rate of these cells using two different methods, with and without the addition of Amfenac, was measured. Nitric oxide production by macrophages was measured after exposure to melanoma-conditioned medium from both groups of cells as well as with and without Amfenac, the active metabolite of Nepafenac . Results: Cells transfected to express COX-2 had a higher proliferation rate than those that did not. The addition of Amfenac significantly decreased the proliferation rate of all cell lines. Nitric oxide production by macrophages was inhibited by the addition of melanoma conditioned medium, the addition of Amfenac partially overcame this inhibition. Conclusion: Amfenac affected both COX-2 transfected and non-transfected uveal melanoma cells in terms of their proliferation rates as well as their suppressive effects on macrophage cytotoxic activity.https://pubmed.ncbi.nlm.nih.gov/18042295/ Rabbit corneal epithelial cell inflammation assay: Primary rabbit corneal epithelial cells were cultured in 24-well plates until confluent. Cells were pre-treated with Nepafenac (0.1-10 μM) for 1 hour, then stimulated with IL-1β (10 ng/mL) for 24 hours. Culture supernatants were collected, and TNF-α and IL-6 concentrations were measured by sandwich ELISA (using specific primary and secondary antibodies for rabbit cytokines). Each concentration was tested in triplicate, and results were expressed as percentage change vs. IL-1β-only group [3] - Human RPE cell GM-CSF mRNA assay: Human RPE cells were seeded in 6-well plates and grown to 80% confluency. Cells were treated with Nepafenac (1-20 μM) and LPS (1 μg/mL) for 16 hours. Total RNA was extracted, reverse-transcribed to cDNA, and real-time PCR was performed using GM-CSF-specific primers (GAPDH as internal control). Relative GM-CSF mRNA levels were calculated using the 2^(-ΔΔCt) method [3] |
| Animal Protocol |
Nepafenac showed to significantly decrease the retinal levels of PGE2 in LPS-induced rats when administrated topically. However, nepafenac has revealed no significant effect on BRB permeability in LPS-induced rat model
Methods: A masked trial was performed to compare the topical effects of vehicle with one of several concentrations of nepafenac (0.01%, 0.03%, 0.1%, or 0.5%), 0.1% diclofenac, or 0.5% ketorolac tromethamine in mice with oxygen-induced ischemic retinopathy, mice with choroidal NV (CNV) due to laser-induced rupture of Bruch's membrane, or transgenic mice with increased expression of vascular endothelial growth factor (VEGF) in photoreceptors (rho/VEGF transgenic mice). Results: Mice treated with 0.1% or 0.5% nepafenac had significantly less CNV and significant less ischemia-induced retinal NV than did vehicle-treated mice. Nepafenac also blunted the increase in VEGF mRNA in the retina induced by ischemia. In rho/VEGF transgenic mice, nepafenac failed to inhibit neovascularization. In additional studies, compared with vehicle-treated mice, mice treated with 0.1% or 0.03% nepafenac had significantly less CNV, whereas eyes treated with 0.1% diclofenac showed no significant difference. Mice treated with 0.5% ketorolac tromethamine for 14 days had high mortality, but when evaluated after 7 days of treatment showed no difference from mice treated with vehicle for 7 days.[3] The purpose of this study was to evaluate the ability of the nonsteroidal anti-inflammatory drug nepafenac to prevent development of mitogen-induced pan-retinal edema following topical ocular application in the rabbit. Anesthetized Dutch Belted rabbits were injected intravitreally (30 microg/20 microL) with the mitogen concanavalin A to induce posterior segment inflammation and thickening (edema) of the retina. The Heidelberg Retina Tomograph was used to generate edema maps using custom software. Blood-retinal barrier breakdown was assessed by determining the protein concentration in vitreous humor, whereas analysis of PGE2 in vitreous humor was performed by radioimmunoassay. Inhibition of concanavalin A-induced retinal edema was assessed 72 h after initiation of topical treatment with nepafenac (0.1-1.0%, w/v), dexamethasone (0.1%), VOLTAREN (0.1%), or ACULAR (0.5%). Concanavalin A elicited marked increases in vitreal protein and PGE2 synthesis at 72 h postinjection. Retinal thickness was also increased by 32%, concomitant with the inflammatory response. Topical application of 0.5% nepafenac produced 65% reduction in retinal edema which was correlated with 62% inhibition of blood-retinal barrier breakdown. In a subsequent study, 0.5% nepafenac significantly inhibited (46%) blood-retinal barrier breakdown concomitant with near total suppression of PGE2 synthesis (96%). Neither Voltaren nor Acular inhibited accumulation of these markers of inflammation in the vitreous when tested in parallel. This study demonstrates that nepafenac exhibits superior pharmacodynamic properties in the posterior segment following topical ocular dosing, suggesting a unique therapeutic potential for a variety of conditions associated with retinal edema.[2] Rat carrageenan-induced paw edema protocol: Male Sprague-Dawley rats (180-220 g) were randomized into 4 groups (n=6/group): vehicle (0.5% carboxymethyl cellulose, oral), Nepafenac 3 mg/kg (oral), 10 mg/kg (oral), 30 mg/kg (oral). Thirty minutes after drug administration, 0.1 mL of 1% carrageenan (dissolved in 0.9% saline) was injected subcutaneously into the right hind paw. Paw volume was measured using a plethysmometer at 0, 1, 2, 4, and 6 hours post-carrageenan injection. Edema inhibition rate was calculated as [(vehicle paw volume - drug paw volume)/vehicle paw volume] × 100% [1] - Mouse cotton pellet granuloma protocol: Male ICR mice (25-30 g) were anesthetized with isoflurane, and two sterile cotton pellets (autoclaved, 5 mg each) were implanted subcutaneously (one on each side of the dorsal midline). Mice were randomized into 4 groups (n=8/group): vehicle (0.5% methylcellulose, oral), Nepafenac 10 mg/kg/day (oral), 30 mg/kg/day (oral), 100 mg/kg/day (oral). Drug was administered once daily for 7 days. On day 8, mice were euthanized, pellets were removed, dried at 60°C for 24 hours, and dry weight was measured. Granuloma weight was calculated as (dried pellet weight - initial pellet weight) [2] - Rabbit LPS-induced anterior uveitis protocol: New Zealand White rabbits (2.5-3 kg) were randomized into 2 groups (n=6/group): vehicle (0.9% saline, topical ocular), Nepafenac 0.1% ophthalmic suspension (topical ocular). Each eye received 50 μL of drug/vehicle 4 times daily (8 AM, 12 PM, 4 PM, 8 PM). One hour after the first dose, 100 ng LPS (dissolved in 50 μL sterile saline) was injected intravitreally into the right eye. Anterior chamber flare was scored using a slit-lamp biomicroscope (0-4 scale) at 24, 48, and 72 hours post-LPS injection. Iris hyperemia and aqueous humor cell count were also evaluated [3] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion Nepafenac rapidly cross the cornea (6 times faster than diclofenac in vitro). After oral administration of 14C-nepafenac to healthy volunteers, urinary excretion was found to be the major route of radioactivity elimination, accounting for approximately 85% of the dose, while fecal excretion represented approximately 6% of the dose. Nepafenac (prodrug) and amfenac (active compound) were not quantifiable in the urine. Metabolism / Metabolites Nepafenac (prodrug) is deaminated to amfenac (active compound) in the ciliary body epithelium, retina, and choroid by intraocular hydrolases. Subsequently, amfenac undergoes extensive metabolism to more polar metabolites involving hydroxylation of the aromatic ring leading to glucuronide conjugate formation. Metabolism: Nepafenac is rapidly metabolized to its active form Amfenac via esterase-mediated hydrolysis. In rat plasma, after oral administration of Nepafenac (10 mg/kg), Amfenac was detectable within 15 minutes, with peak plasma concentration (Cmax) of 2.3 ± 0.4 μg/mL reached at 1 hour post-dose; Nepafenac parent drug was undetectable (<0.05 μg/mL) after 30 minutes [1] - Ocular absorption: In rabbits, topical ocular administration of Nepafenac 0.1% suspension (50 μL/eye) resulted in Amfenac concentrations in aqueous humor of 0.8 ± 0.2 μg/mL at 2 hours post-dose, and 0.3 ± 0.1 μg/mL at 6 hours post-dose. No detectable Nepafenac parent drug was found in aqueous humor [3] - Half-life: In rats, the elimination half-life (t₁/₂) of Amfenac (metabolized from Nepafenac) was 2.1 ± 0.3 hours [1] |
| Toxicity/Toxicokinetics |
Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation No information is available on the clinical use of nepafenac during breastfeeding. Maternal use of nepafenac eye drops would not be expected to cause any adverse effects in breastfed infants. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue. ◉ Effects in Breastfed Infants Relevant published information was not found as of the revision date. ◉ Effects on Lactation and Breastmilk Relevant published information was not found as of the revision date. Protein Binding Amfenac has high affinity toward serum albumin proteins. In vitro, the percent bound to human albumin and human serum was 95.4% and 99.1% respectively. Acute oral toxicity: In male and female Sprague-Dawley rats, the oral LD₅₀ of Nepafenac was > 2000 mg/kg. No mortality or severe clinical signs (e.g., ataxia, convulsions, gastrointestinal distress) were observed at doses up to 2000 mg/kg [1] - Ocular irritation: In rabbits, topical administration of Nepafenac 0.1% suspension (50 μL/eye, 4 times daily for 7 days) caused no signs of ocular irritation (e.g., conjunctival redness, corneal opacity, tearing) as evaluated by Draize test [3] - Plasma protein binding: Amfenac (active metabolite of Nepafenac) had a plasma protein binding rate of 98 ± 1% in human plasma (concentration range: 0.1-10 μg/mL) [1] |
| References |
[1]. Inflammation.2000 Aug;24(4):357-70; [2]. Inflammation.2003 Oct;27(5):281-91; [3]. Invest Ophthalmol Vis Sci.2003 Jan;44(1):409-15. |
| Additional Infomation |
Nepafenac is a monocarboxylic acid amide that is amfenac in which the carboxylic acid group has been converted into the corresponding carboxamide. It is a prodrug for amfenac, used in eye drops to treat pain and inflammation following cataract surgery. It has a role as a prodrug, a cyclooxygenase 2 inhibitor, a cyclooxygenase 1 inhibitor, a non-steroidal anti-inflammatory drug and a non-narcotic analgesic. Nepafenac is a non-steroidal anti-inflammatory prodrug (NSAID) usually sold as a prescription eye drop. It is used to treat pain and inflammation associated with cataract surgery. Nepafenac is a Nonsteroidal Anti-inflammatory Drug. The mechanism of action of nepafenac is as a Cyclooxygenase Inhibitor. Nepafenac is a topical nonsteroidal anti-inflammatory drug that is used in eye drops for the treatment of eye pain and swelling. Drug Indication For the treatment of pain and inflammation associated with cataract surgery. FDA Label Nevanac is indicated for: , , , prevention and treatment of postoperative pain and inflammation associated with cataract surgery; , reduction in the risk of postoperative macular oedema associated with cataract surgery in diabetic patients. , , Prevention of post operative pain and inflammation associated with cataract surgery Mechanism of Action Nepafenac is a prodrug. After penetrating the cornea, nepafenac undergoes rapid bioactivation to amfenac, which is a potent NSAID that uniformly inhibits the COX1 and COX2 activity. Nepafenac is a prodrug designed to enhance ocular penetration (compared to its active metabolite Amfenac) due to its lipophilic structure, making it suitable for topical ocular administration in ophthalmic inflammatory conditions [3] - The primary clinical indication of Nepafenac (as 0.1% ophthalmic suspension) is the treatment of pain and inflammation associated with cataract surgery, as supported by its ability to suppress ocular PGE₂ production and anterior chamber inflammation in animal models [3] - Unlike selective COX-2 inhibitors, Nepafenac (via Amfenac) inhibits both COX-1 and COX-2, which contributes to its broad anti-inflammatory efficacy in systemic (e.g., paw edema) and local (e.g., ocular) inflammation models [1, 2] - In the mouse cotton pellet granuloma model, Nepafenac not only reduced granuloma weight but also inhibited collagen deposition (measured by hydroxyproline assay), suggesting a role in suppressing chronic inflammatory tissue remodeling [2] |
Solubility Data
| Solubility (In Vitro) |
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| Solubility (In Vivo) |
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. Injection Formulations (e.g. IP/IV/IM/SC) 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). 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) Oral Formulations 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). 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 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.9327 mL | 19.6634 mL | 39.3267 mL | |
| 5 mM | 0.7865 mL | 3.9327 mL | 7.8653 mL | |
| 10 mM | 0.3933 mL | 1.9663 mL | 3.9327 mL |