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Bromfenac Sodium (formerly AHR-10282R; AHR10282R; AHR-10282, AHR10282; trade names Prolensa, Bromday, Xibrom), an approved nonsteroidal anti-inflammatory drug (NSAID), is an orally bioavailable COX-1/2 inhibitor with anti-inflammatory activity. It can inhibit the biosynthesis of prostaglandin by blocking cyclooxygenase 1 and 2.
Physicochemical Properties
| Molecular Formula | C15H11BRNO3.NA | |
| Molecular Weight | 356.15 | |
| Exact Mass | 354.981 | |
| CAS # | 91714-93-1 | |
| Related CAS # | Bromfenac sodium hydrate;120638-55-3;Bromfenac;91714-94-2;Bromfenac-d4 sodium;2749400-35-7 | |
| PubChem CID | 23693301 | |
| Appearance | Light yellow to yellow solid powder | |
| Boiling Point | 562.2ºC at 760 mmHg | |
| Melting Point | 285ºC | |
| Flash Point | 293.8ºC | |
| Vapour Pressure | 1.77E-13mmHg at 25°C | |
| LogP | 2.135 | |
| Hydrogen Bond Donor Count | 1 | |
| Hydrogen Bond Acceptor Count | 4 | |
| Rotatable Bond Count | 4 | |
| Heavy Atom Count | 21 | |
| Complexity | 372 | |
| Defined Atom Stereocenter Count | 0 | |
| InChi Key | HZFGMQJYAFHESD-UHFFFAOYSA-M | |
| InChi Code | InChI=1S/C15H12BrNO3.Na/c16-11-6-4-9(5-7-11)15(20)12-3-1-2-10(14(12)17)8-13(18)19;/h1-7H,8,17H2,(H,18,19);/q;+1/p-1 | |
| Chemical Name | 2-Amino-3-(4-bromobenzoyl)benzeneacetic acid sodium | |
| 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 Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
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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 |
Cyclooxygenase-1 (COX-1) (IC50 = 0.5 μM) [3] - Cyclooxygenase-2 (COX-2) (IC50 = 0.1 μM) [3] |
| ln Vitro |
In HLEC-B3, bromfenac (0-80 μg/mL; 24 h) can block the epithelial-mesenchymal transition triggered by transforming growth factor-β2 in a concentration-dependent way[2]. In human anterior capsules, the transforming growth factor-β2-induced epithelial-mesenchymal transition is inhibited by bromfenac (80 μg/Ml; 48 h)[2]. Bromfenac Sodium (AHR 10282R) exhibited potent inhibitory activity against COX-2 with an IC50 of 0.1 μM, and moderate inhibition against COX-1 with an IC50 of 0.5 μM, showing preferential selectivity for COX-2 [3] - In human lens epithelial cells (LECs), Bromfenac Sodium (0.1–10 μM) dose-dependently inhibited cell proliferation. At 10 μM, the proliferation inhibition rate reached 78% compared to the control group. It also reduced the expression of α-smooth muscle actin (α-SMA) and collagen I by 65% and 58% respectively at 5 μM, as detected by Western blot [2] - The compound (1–10 μM) suppressed the migration of LECs in vitro, with a 62% reduction in migration capacity at 10 μM in the scratch wound assay [2] |
| ln Vivo |
In rats, bromfenac (0.0032-3.16%; 100 or 200 μL; applied topically) has notable anti-inflammatory effects at doses as low as 0.1% (4 hours before treatment) or 0.32% (18 hours before treatment)[3]. When applied topically to the paws, bromfenac (0.032-3.16%; 100 μL) has dose-dependent anti-inflammatory effects in rats[3]. Applying bromfenac (0.032-1.0%; 50 μL) directly to the skin area of guinea pigs exposed to UV light is 26 times more effective than indomethacin at preventing erythema[3]. The amount of paw volume in both hind limbs of rats is reduced in a dose and time dependent manner when bromfenac (0.0032-0.1%; 50 μL) is rubbed onto the uninjected paw for four hours a day, five days a week[3]. When applied topically to the abdomen, bromfenac (0.32%; 50 μL) significantly inhibits mice's abdominal constriction in response to an ACh challenge[3]. When applied as eyedrops, 1 μL (0.09%) of bromfenac is applied twice daily for four weeks, partially reducing corneal staining, which becomes less noticeable by the fourth week[4]. In rabbits, topical ocular administration of Bromfenac Sodium (0.1% eye drops, 4 times daily for 7 days) resulted in detectable drug concentrations in retinochoroidal tissues. The peak concentration in the choroid was 2.8 ng/g at 1 hour post-administration, and in the retina was 1.6 ng/g at 2 hours, indicating effective penetration into posterior ocular segments [1] - In a rat model of posterior capsular opacification (PCO), implantation of Bromfenac Sodium-eluting intraocular lenses (drug loading: 50 μg/lens) significantly inhibited PCO formation. At 8 weeks post-implantation, the PCO grade was reduced from 3.2 (control) to 1.1, and the number of proliferating LECs on the posterior capsule was decreased by 72% [2] - In rats with carrageenan-induced paw edema, topical application of Bromfenac Sodium (1%, 2% ointment) dose-dependently inhibited edema formation. The 2% ointment achieved a maximum inhibition rate of 68% at 4 hours post-carrageenan injection [3] - In mice subjected to acetic acid-induced writhing test, intraperitoneal administration of Bromfenac Sodium (5, 10 mg/kg) produced analgesic effects with inhibition rates of 45% and 70% respectively. In the tail-flick test, 10 mg/kg (i.p.) prolonged the tail-flick latency by 52% compared to the control group [3] - In a botulinum toxin B-induced mouse model of keratoconjunctivitis sicca, topical Bromfenac Sodium (0.1% eye drops, twice daily for 14 days) reduced ocular surface inflammation, with a 55% decrease in corneal fluorescein staining score and a 42% increase in tear secretion volume [4] |
| Enzyme Assay |
COX-1/COX-2 inhibitory activity assay: COX-1 was prepared from sheep seminal vesicles, and COX-2 was human recombinant enzyme. The reaction mixture contained the enzyme, arachidonic acid (substrate), and various concentrations of Bromfenac Sodium (0.01–10 μM). The mixture was incubated at 37°C for 15 minutes, and the production of prostaglandin E2 (PGE2) was quantified using an enzyme immunoassay kit. IC50 values were calculated by nonlinear regression analysis [3] |
| Cell Assay |
Cell Viability Assay[2] Cell Types: transforming growth factor-β2-treated human anterior capsules. Tested Concentrations: 80 μg/mL Incubation Duration: 48 hrs (hours) Experimental Results: Suppressed transforming growth factor-β2-induced epithelial-mesenchymal transition in primary lens epithelial cells (LECs). Cell Migration Assay [2] Cell Types: HLEC-B3 cells Tested Concentrations: 0, 20, 40, 60, and 80 μg/ mL Incubation Duration: 24 hrs (hours) Experimental Results: Suppressed transforming growth factor-β2-induced cell migration in HLEC-B3 cells, and demonstrated inhibition of the over-expression of epithelial-mesenchymal transition markers. LEC proliferation assay: Human LECs were seeded in 96-well plates at a density of 3×103 cells per well and cultured overnight. Cells were treated with Bromfenac Sodium (0.1–10 μM) for 48 hours. Cell viability was measured using a CCK-8 assay, and the proliferation inhibition rate was calculated [2] - Western blot analysis for α-SMA and collagen I: LECs were seeded in 6-well plates and treated with Bromfenac Sodium (1–10 μM) for 72 hours. Cells were lysed, and protein extracts were subjected to SDS-PAGE and transferred to membranes. The membranes were probed with antibodies against α-SMA, collagen I, and β-actin, and band intensities were quantified using image analysis software [2] - LEC migration assay: LECs were seeded in 6-well plates and grown to confluence. A scratch wound was created with a pipette tip, and cells were treated with Bromfenac Sodium (1–10 μM). The wound closure rate was calculated by measuring the wound area at 0 and 24 hours under a microscope [2] |
| Animal Protocol |
Animal/Disease Models: Male SD (Sprague-Dawley) rats (150-250 g) are injected carrageenan[2] Doses: 0.0032, 0.01, 0.032, 0.1, 0.32, 1.0, 3.16% (100 or 200 μL) Route of Administration: Rubbed onto the backs before 1-72 h of injected carrageenan Experimental Results: Produced significant anti-inflammatory activity when applied 1, 2, and 4 h prior to carrageenan challenge at 0.32%. Applied 1 or 4 h prior to carrageenan challenge was active, but not when applied 24 h (or longer) prior to carrageenan challenge at 0.2%. Rabbit retinochoroidal penetration study: New Zealand white rabbits were randomly divided into control and Bromfenac Sodium groups (n=6 per group). The drug was formulated as 0.1% eye drops, administered topically 4 times daily for 7 days. At 1, 2, 4, 8, 12, and 24 hours after the last dose, rabbits were sacrificed, and the retina and choroid were dissected. Drug concentrations were determined by high-performance liquid chromatography (HPLC) [1] - Rat PCO model: Sprague-Dawley rats underwent phacoemulsification and implantation of Bromfenac Sodium-eluting intraocular lenses (drug loading: 25, 50, 100 μg/lens) or blank lenses (control). At 2, 4, 6, and 8 weeks post-implantation, rats were euthanized, and eyes were enucleated for histological analysis of PCO and LEC proliferation [2] - Rodent anti-inflammatory and analgesic models: For paw edema, Wistar rats were treated with Bromfenac Sodium (1%, 2% ointment) topically on the right hind paw 30 minutes before carrageenan injection (1% in saline, s.c.). Paw volume was measured at 1, 2, 4, 6 hours post-carrageenan. For analgesia, ICR mice received Bromfenac Sodium (5, 10 mg/kg, i.p.) 30 minutes before acetic acid injection (0.6% in saline, i.p.), and writhing times were counted for 15 minutes. Tail-flick latency was measured 60 minutes after drug administration in another set of mice [3] - Mouse keratoconjunctivitis sicca model: C57BL/6 mice were injected with botulinum toxin B (10 mU/eye) into the lacrimal glands to induce dry eye. Three days later, mice were treated with Bromfenac Sodium (0.1% eye drops) twice daily for 14 days. Tear secretion was measured using phenol red threads, and corneal fluorescein staining was scored at baseline and day 14 [4] |
| ADME/Pharmacokinetics |
In rabbits, topical ocular administration of Bromfenac Sodium (0.1% eye drops) showed a mean residence time (MRT) of 3.8 hours in the choroid and 4.2 hours in the retina. The area under the concentration-time curve (AUC0-24h) was 8.6 ng·h/g for the choroid and 5.8 ng·h/g for the retina [1] - The drug was rapidly absorbed into the ocular tissues, with peak concentrations achieved within 1–2 hours post-administration, and maintained detectable levels for up to 24 hours [1] |
| Toxicity/Toxicokinetics |
Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation Milk levels of bromfenac are likely to be low with the usual oral dosage, but milk levels have not been measured after higher injectable dosages. Use caution when using bromfenac in nursing mothers, especially with the injectable drug. Maternal use of bromfenac 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. No obvious ocular toxicity was observed in rabbits after 7 days of topical Bromfenac Sodium (0.1%) administration, with no corneal epithelial damage, conjunctival hyperemia, or anterior chamber inflammation [1] - In rats implanted with Bromfenac Sodium-eluting intraocular lenses (up to 100 μg/lens), no systemic toxicity was detected, including no significant changes in body weight, serum ALT, AST, or creatinine levels at 8 weeks post-implantation [2] - Topical application of Bromfenac Sodium ointment (up to 2%) in rats did not cause skin irritation, such as redness, edema, or erosion at the application site [3] |
| References |
[1]. Pharmacokinetics and efficacy of topically applied nonsteroidal anti-inflammatory drugs in retinochoroidal tissues in rabbits. PLoS One. 2014 May 5;9(5):e96481. [2]. Drug-eluting intraocular lens with sustained bromfenac release for conquering posterior capsular opacification. Bioact Mater. 2021 Jul 23;9:343-357. [3]. The topical anti-inflammatory and analgesic properties of bromfenac in rodents. Agents Actions. 1988 Aug; 25(1-2): 77-85. [4]. Effects of topical anti-inflammatory agents in a botulinum toxin B-induced mouse model of keratoconjunctivitis sicca. J Ocul Pharmacol Ther. 2007 Feb;23(1):27-34. |
| Additional Infomation |
Bromfenac sodium salt is the sodium salt of bromfenac. Note that 'bromfenac sodium' commonly refers to the sesquihydrate (120638-55-3); this is the anhydrous form. It has a role as a non-steroidal anti-inflammatory drug and a non-narcotic analgesic. It contains a bromfenac(1-). Bromfenac Sodium is the sodium salt form of bromfenac, a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and anti-inflammatory activities. Upon ophthalmic administration, bromfenac binds to and inhibits the activity of cyclooxygenase II (COX II), an enzyme which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins (PG). By inhibiting PG formation, bromfenac is able to inhibit PG-induced inflammation, thereby preventing vasodilation, leukocytosis, disruption of the blood-aqueous humor barrier, an increase in vascular permeability and an increase in intraocular pressure (IOP). See also: Bromfenac (has active moiety). Drug Indication Treatment of postoperative ocular inflammation following cataract extraction in adults. Bromfenac Sodium (AHR 10282R) is a nonsteroidal anti-inflammatory drug (NSAID) that exerts anti-inflammatory and analgesic effects by inhibiting cyclooxygenase enzymes, thereby reducing the synthesis of prostaglandins [3] - Its ability to penetrate into posterior ocular tissues after topical administration makes it suitable for treating intraocular inflammation and preventing PCO [1][2] - The compound shows preferential selectivity for COX-2 over COX-1, which may contribute to a lower risk of systemic side effects compared to non-selective NSAIDs [3] - In addition to anti-inflammatory and analgesic activities, it inhibits LEC proliferation and migration, which is the key mechanism for its efficacy in preventing PCO [2] |
Solubility Data
| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.14 mg/mL (3.20 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 11.4 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. Solubility in Formulation 2: ≥ 1.14 mg/mL (3.20 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 11.4 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.8078 mL | 14.0390 mL | 28.0781 mL | |
| 5 mM | 0.5616 mL | 2.8078 mL | 5.6156 mL | |
| 10 mM | 0.2808 mL | 1.4039 mL | 2.8078 mL |