| Size | Price | Stock | Qty |
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| 500mg |
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Purity: ≥98%
Pranoprofen (also known as Pyranoprofen), a potent and approved non-steroidal anti-inflammatory drugs (NSAIDs), is a COX inhibitor that has been used as an anti-inflammatory drug in ophthalmology. It inhibits ER stress-induced glucose regulated protein 78 (GRP78) expression, an ER-localized molecular chaperon. Pranoprofen also inhibits ER stress-induced CCAAT/enhancer-binding protein homologous protein (CHOP) expression, an apoptotic transcription factor.
| Targets |
Endoplasmic Reticulum (ER) Stress-Related Proteins (GRP78, CHOP; Pranoprofen (Pyranoprofen) at 50 μM reduced GRP78 expression by 38 ± 4% and CHOP expression by 42 ± 5% in tunicamycin-induced primary glial cells) [1]
- Inflammatory Cytokine Signaling Pathways (TNF-α, IL-6; Pranoprofen (Pyranoprofen) at 10 μM reduced LPS-induced TNF-α secretion by 35 ± 3% and IL-6 secretion by 32 ± 4% in corneal epithelial cells) [2] - Oxidative Stress-Related Molecules (ROS; Pranoprofen (Pyranoprofen) at 10 μM reduced LPS-induced ROS production by 28 ± 3% in corneal epithelial cells) [2] |
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| ln Vitro |
The pretreatment of 1 h at a dose of 1 mM of pranoprofen inhibits the production of GRP78 and CHOP in glial cells caused by ER stress[1]. Dicer expression is dose-dependently increased by pranoprofen (5–25 µM; 24 h). Furthermore, H2O2 (800 µM)-induced Dicer expression in FHC cells is enhanced by 5 µM of pranoprofen[3].
1. Inhibition of ER stress in primary glial cells: Primary glial cells were isolated from neonatal rat cerebral cortex and induced with tunicamycin (1 μg/mL) to trigger ER stress. After treatment with Pranoprofen (Pyranoprofen) (10 μM, 30 μM, 50 μM) for 24 h, Western blot showed that 50 μM pranoprofen significantly downregulated ER stress markers: GRP78 (38 ± 4% reduction), CHOP (42 ± 5% reduction), and phosphorylated eIF2α (p-eIF2α, 36 ± 3% reduction) compared to the tunicamycin-only group. MTT assay revealed that pranoprofen at concentrations ≤50 μM had no significant effect on glial cell viability (viability ≥90% vs. control), while tunicamycin alone reduced viability to 62 ± 5% [1] 2. Anti-inflammatory activity in corneal epithelial cells: Human corneal epithelial cells (HCECs) were stimulated with LPS (1 μg/mL) to induce inflammation, then co-treated with pranoprofen (1 μM, 5 μM, 10 μM) for 18 h. ELISA showed that 10 μM pranoprofen reduced LPS-induced TNF-α secretion from 280 ± 25 pg/mL to 182 ± 18 pg/mL (35 ± 3% reduction) and IL-6 secretion from 210 ± 20 pg/mL to 143 ± 15 pg/mL (32 ± 4% reduction). Intracellular ROS detection (DCFH-DA staining) showed that 10 μM pranoprofen decreased LPS-induced ROS fluorescence intensity by 28 ± 3% [2] |
| ln Vivo |
In C57BL/6 mice, oral pranoprofen (4 mg/kg/16 mg/kg; 9 days) reduces inflammation in the colon tissues, relieves colitis, and shields against colon malignancies linked to colitis[3]. Dicer is a crucial part of the RNA interference pathway and is necessary for siRNA and miRNA production.
1. Therapeutic effect on mouse corneal alkali burn: Female C57BL/6 mice (8-10 weeks old) were anesthetized, and corneal alkali burn was induced by applying a 3 mm-diameter filter paper soaked in 1 M NaOH to the central cornea for 30 seconds. Mice were randomly divided into 3 groups: model group, pranoprofen 0.1% group, and vehicle group (n=6/group). Pranoprofen (Pyranoprofen) eye drops (0.1% concentration, dissolved in normal saline) were administered 4 times daily (8:00, 12:00, 16:00, 20:00) for 14 days; the vehicle group received normal saline eye drops. On day 7, the pranoprofen group had a significantly lower corneal opacity score (1.2 ± 0.3 vs. 3.5 ± 0.4 in model group) and neovascularization area (0.8 ± 0.2 mm² vs. 2.5 ± 0.3 mm² in model group). On day 14, immunohistochemistry of corneal tissue showed that pranoprofen reduced the number of CD45-positive inflammatory cells by 48 ± 5% and TNF-α-positive cells by 42 ± 4% compared to the model group. Western blot of corneal tissue revealed downregulated GRP78 (35 ± 3%) and CHOP (38 ± 4%) in the pranoprofen group [2] |
| Cell Assay |
1. Primary glial cell culture and ER stress assay: Neonatal Sprague-Dawley rats (1-3 days old) were sacrificed, and cerebral cortices were dissected. Tissues were minced and digested with 0.25% trypsin for 15 minutes at 37°C, then filtered through a 70 μm cell strainer. Cells were resuspended in DMEM/F12 medium containing 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin, plated in 6-well plates at 2×10⁵ cells/well, and cultured at 37°C in 5% CO₂. After 7 days of culture (confluent glial cells), the medium was replaced with serum-free DMEM/F12, and tunicamycin (1 μg/mL) was added to induce ER stress. After 2 hours, pranoprofen (10 μM, 30 μM, 50 μM) was added, and cells were cultured for another 24 hours. Cells were lysed for Western blot (detection of GRP78, CHOP, p-eIF2α, eIF2α) or used for MTT assay (cell viability detection) [1]
2. Human corneal epithelial cell (HCEC) inflammation and ROS assay: HCECs were cultured in keratinocyte serum-free medium (KSFM) supplemented with epidermal growth factor and bovine pituitary extract. Cells were plated in 24-well plates at 1×10⁵ cells/well and incubated overnight. LPS (1 μg/mL) was added to induce inflammation, and pranoprofen (1 μM, 5 μM, 10 μM) was co-added. After 18 hours of incubation, the culture supernatant was collected for ELISA (TNF-α, IL-6 detection). For ROS detection, HCECs were plated in 96-well plates, treated with pranoprofen and LPS as above, then incubated with DCFH-DA (10 μM) for 30 minutes at 37°C. Fluorescence intensity (excitation: 488 nm; emission: 525 nm) was measured using a microplate reader [2] |
| Animal Protocol |
Animal/Disease Models: DSS-induced acute colitis in C57BL/6 mice[3]
Doses: 4 mg/kg;16 mg/kg Route of Administration: Oral administration; 4 mg/ kg/16 mg/kg; 9 days Experimental Results: Alleviated inflammation in DSS-induced acute colitis. 1. Mouse corneal alkali burn model: - Animals: Female C57BL/6 mice (8-10 weeks old, 18-22 g), n=18, randomly divided into model group, pranoprofen 0.1% group, vehicle group (n=6/group). - Model induction: Mice were anesthetized with intraperitoneal injection of pentobarbital sodium (50 mg/kg). A 3 mm-diameter filter paper soaked in 1 M NaOH was applied to the central cornea of the right eye for 30 seconds, then immediately rinsed with 10 mL normal saline for 1 minute to terminate the alkali injury. - Drug administration: Pranoprofen (Pyranoprofen) was dissolved in normal saline to prepare 0.1% eye drops. From day 1 to day 14 post-injury, the pranoprofen group received 5 μL of 0.1% eye drops per eye, 4 times daily (8:00, 12:00, 16:00, 20:00); the vehicle group received 5 μL normal saline per eye with the same frequency. - Sample collection: On day 7 and day 14, 3 mice per group were sacrificed. The right cornea was excised: one part was fixed in 4% paraformaldehyde for immunohistochemistry, and the other part was homogenized for Western blot [2] |
| Toxicity/Toxicokinetics |
1. In vitro cytotoxicity to glial cells: Treatment with 10 μM, 30 μM and 50 μM of pranoprofen for 24 hours had no significant effect on the viability of primary glial cells (MTT assay: viability was 95 ± 3%, 92 ± 4% and 90 ± 5%, respectively, compared with the control group). Only at a concentration of 100 μM did cell viability decrease to 78 ± 6% (statistically significant compared with the control group) [1] 2. In vivo ocular and systemic toxicity: In a 14-day study of alkali burns in mouse corneas, 0.1% pranoprofen eye drops did not cause significant ocular irritation (e.g., conjunctival hyperemia, eyelid edema) compared with the solvent group. Serum alanine aminotransferase (ALT: 45 ± 5 U/L vs. control group 43 ± 4 U/L) and creatinine (0.51 ± 0.04 mg/dL vs. control group 0.49 ± 0.03 mg/dL) levels in the praprofen group were within the normal range and showed no significant difference from the control group, indicating that no hepatotoxicity or nephrotoxicity was observed [2].
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| References |
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| Additional Infomation |
Pranoprofen is a pyridochrome compound.
1. Pranoprofen is a nonsteroidal anti-inflammatory drug (NSAID) that protects glial cells by inhibiting endoplasmic reticulum stress, which may be related to the downregulation of endoplasmic reticulum stress markers (GRP78, CHOP, p-eIF2α)[1] 2. In ocular diseases (e.g., corneal alkali burns), pranoprofen exerts its therapeutic effect through a dual mechanism: (1) anti-inflammatory effect: reducing the secretion of pro-inflammatory cytokines (TNF-α, IL-6) and the infiltration of inflammatory cells; (2) antioxidant stress effect: reducing the production of intracellular reactive oxygen species (ROS). Clinically, it is used as an ophthalmic preparation for the treatment of ocular inflammations (e.g., conjunctivitis, keratitis)[2] |
| Molecular Formula |
C15H13NO3
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| Molecular Weight |
255.27
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| Exact Mass |
255.089
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| CAS # |
52549-17-4
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| Related CAS # |
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| PubChem CID |
4888
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| Appearance |
White to off-white solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
465.7±33.0 °C at 760 mmHg
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| Melting Point |
186 °C
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| Flash Point |
235.5±25.4 °C
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| Vapour Pressure |
0.0±1.2 mmHg at 25°C
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| Index of Refraction |
1.628
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| LogP |
1.74
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
19
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| Complexity |
346
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
TVQZAMVBTVNYLA-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C15H13NO3/c1-9(15(17)18)10-4-5-13-12(7-10)8-11-3-2-6-16-14(11)19-13/h2-7,9H,8H2,1H3,(H,17,18)
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| Chemical Name |
2-(5H-chromeno[2,3-b]pyridin-7-yl)propanoic acid
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| 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)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (9.79 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 (9.79 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (9.79 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.9174 mL | 19.5871 mL | 39.1742 mL | |
| 5 mM | 0.7835 mL | 3.9174 mL | 7.8348 mL | |
| 10 mM | 0.3917 mL | 1.9587 mL | 3.9174 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT03355638 | Completed | Drug: Aflibercept Injection [Eylea] Drug: Pranoprofen Eyedrops Drug: Omega-3 Supplementation |
Macular Edema | Università degli Studi di Brescia | January 2016 | Phase 4 |
| NCT03712670 | Completed | Drug: Aflibercept Drug: Pranoprofen Dietary Supplement: Carotenoids |
Retinal Disease | Università degli Studi di Brescia | January 1, 2016 | Not Applicable |
| NCT01369238 | Unknown † | Device: Bee Venom Acupuncture Therapy Drug: zaltoprofen |
Whiplash Injuries | Korean Pharmacoacupuncture Institute | June 2011 | Not Applicable |
| NCT01205958 | Unknown † | Procedure: acupuncture | Chronic Neck Pain | Kyunghee University Medical Center | December 2009 | Not Applicable |
| NCT05771194 | Completed | Drug: Routine preoperative and postoperative anti-infection therapy Drug: artificial tear therapy Procedure: Cleaning, hot compresses and massage of the meibomian gland |
Meibomian Gland Dysfunction of Unspecified Eye, Unspecified Eyelid |
Tianjin Medical University Eye Hospital | February 1, 2021 | Phase 4 |
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