Roflumilast (Synonyms: B 9302107, BY 217, BYK 20869) |
Katalog-Nr.GC16347
One-Click Copy Product Info
|
Roflumilast is an orally active selective phosphodiesterase-4 (PDE-4) inhibitor that inhibits the activity of PDE4A1 (IC50=0.7nM), PDE4A4 (IC50=0.9nM), PDE4B1 (IC50=0.7nM), and PDE4B2 (IC50=0.2nM).
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 162401-32-3
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
Roflumilast is an orally active selective phosphodiesterase-4 (PDE-4) inhibitor that inhibits the activity of PDE4A1 (IC50=0.7nM), PDE4A4 (IC50=0.9nM), PDE4B1 (IC50=0.7nM), and PDE4B2 (IC50=0.2nM). By inhibiting PDE-4, Roflumilast increases intracellular cyclic adenosine monophosphate (cAMP) levels, thereby activating the protein kinase A (PKA) pathway and suppressing the production of pro-inflammatory mediators. Roflumilast can be used in research related to chronic obstructive pulmonary disease and inflammatory skin diseases (such as plaque psoriasis and atopic dermatitis)[1-4].
In vitro, Roflumilast (15μM) was used to treat OVCAR3 and SKOV3 ovarian cancer cells for 24 hours. Roflumilast enhanced cellular sensitivity to cisplatin, inhibited cell proliferation, induced apoptosis and G0/G1 phase arrest, and upregulated the expression of mitochondrial ferritin (FtMt) by activating the cAMP/PKA/CREB signaling pathway[5]. Roflumilast (3–6μM) was applied to 3T3-L1 preadipocytes in adipogenic differentiation medium for 8 days. Roflumilast inhibited lipid accumulation and triglyceride storage, promoted lipolysis, downregulated the expression of adipogenic genes (SREBP1C, FABP4, Glut4) and their regulators (PPAR-γ and C/EBPα), and exerted its effects through activation of the AMPKα pathway[6].
In vivo, Roflumilast (5mg/kg/day) was intraperitoneally injected into STK11KO pancreatic cancer model C57BL/6 mice for 16 days. Roflumilast significantly reduced pancreatic tumor weight and impeded pancreatic cancer progression[7]. A/J mice that had received intraperitoneal injections of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; 100mg/kg) for two weeks were treated with Roflumilast (5mg/kg/day; 5 days per week; intragastric gavage) and cigarette smoke (1 hour per day, 5 days per week; inhalation) for 20 weeks. Roflumilast significantly reduced the incidence of lung adenocarcinomas, alleviated pulmonary inflammation, and mitigated emphysema in the mice[8].
References:
[1] Hatzelmann A, Morcillo EJ, Lungarella G, et al. The preclinical pharmacology of roflumilast--a selective, oral phosphodiesterase 4 inhibitor in development for chronic obstructive pulmonary disease. Pulm Pharmacol Ther. 2010 Aug;23(4):235-56.
[2] Rabe KF. Update on roflumilast, a phosphodiesterase 4 inhibitor for the treatment of chronic obstructive pulmonary disease. Br J Pharmacol. 2011 May;163(1):53-67.
[3] Sanz MJ, Cortijo J, Taha MA, et al. Roflumilast inhibits leukocyte-endothelial cell interactions, expression of adhesion molecules and microvascular permeability. Br J Pharmacol. 2007 Oct;152(4):481-92.
[4] Abdel-Wahab BA, Walbi IA, Albarqi HA, et al. Roflumilast protects from cisplatin-induced testicular toxicity in male rats and enhances its cytotoxicity in prostate cancer cell line. Role of NF-κB-p65, cAMP/PKA and Nrf2/HO-1, NQO1 signaling. Food Chem Toxicol. 2021 May;151:112133.
[5] Gong S, Chen Y, Meng F, et al. Roflumilast enhances cisplatin-sensitivity and reverses cisplatin-resistance of ovarian cancer cells via cAMP/PKA/CREB-FtMt signalling axis. Cell Prolif. 2018 Oct;51(5):e12474.
[6] Xu W, Zhang J, Xiao J. Roflumilast Suppresses Adipogenic Differentiation via AMPK Mediated Pathway. Front Endocrinol (Lausanne). 2021 Jun 7;12:662451.
[7] Zhang S, Yun D, Yang H, et al. Roflumilast inhibits tumor growth and migration in STK11/LKB1 deficient pancreatic cancer. Cell Death Discov. 2024 Mar 9;10(1):124.
[8] Sakurai K, Nakayama S, Chubachi S, et al. Roflumilast reduces the number of lung adenocarcinomas, inflammation, and emphysema in a smoking-induced mouse model. BMC Pulm Med. 2025 May 26;25(1):262.
| Cell experiment [1]: | |
Cell lines | 3T3-L1 preadipocytes (mouse preadipocyte cell line) |
Preparation Method | 3T3-L1 preadipocytes were seeded in 12-well culture plates with complete medium (high glucose Dulbecco's Modified Eagle Medium, 10% fetal bovine serum, and 50μg/ml penicillin/streptomycin). Upon confluence, the media were replaced with an adipogenic differentiation cocktail containing 0.5mM 3-isobutyl-1-methylxanthine (IBMX) and 1mM dexamethasone. Roflumilast (3-6μM) was incorporated into the induction medium. |
Reaction Conditions | 3-6μM; 8 days (during adipogenic differentiation) |
Applications | Roflumilast inhibited lipid accumulation and triglycerides storage in mature 3T3-L1 cells. Roflumilast decreased the differentiation-induced expression of adipogenesis genes including SREBP1C, FABP4, and Glut4, as well as their regulators including PPAR-γ and C/EBPα. Roflumilast promoted lipolysis (glycerol release). The effect of Roflumilast was dependent on the activation of AMPKα. |
| Animal experiment [2]: | |
Animal models | Male A/J mice (7-10 weeks old) |
Preparation Method | Mice were intraperitoneally injected with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (100mg/kg). After 2 weeks, they were exposed to intermittent mainstream cigarette smoke (1 hour per day, 5 days per week) for 20 weeks. Roflumilast (5mg/kg) was administered via intragastric gavage once daily (5 days per week) for 20 weeks during the smoke exposure period. |
Dosage form | 5mg/kg; gavage; once daily for 5 days a week for 20 weeks |
Applications | Roflumilast reduced the number of lung tumors, particularly adenocarcinomas, induced by intermittent smoking exposure. Roflumilast attenuated the increase in total cells and macrophages in bronchoalveolar lavage fluid and suppressed smoking-induced expressions of inflammatory cytokines (IL-6, IL-1β, and TNF-α) in lung tissue. Roflumilast also reduced emphysematous changes (lower mean linear intercept and destructive index). |
References: | |
| Cas No. | 162401-32-3 | SDF | |
| Überlieferungen | B 9302107, BY 217, BYK 20869 | ||
| Chemical Name | 3-(cyclopropylmethoxy)-N-(3,5-dichloropyridin-4-yl)-4-(difluoromethoxy)benzamide | ||
| Canonical SMILES | C1CC1COC2=C(C=CC(=C2)C(=O)NC3=C(C=NC=C3Cl)Cl)OC(F)F | ||
| Formula | C17H14Cl2F2N2O3 | M.Wt | 403.21 |
| Löslichkeit | ≥ 20.2 mg/mL in DMSO, ≥ 9.94 mg/mL in EtOH with ultrasonic | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
||
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 2.4801 mL | 12.4005 mL | 24.801 mL |
| 5 mM | 496 μL | 2.4801 mL | 4.9602 mL |
| 10 mM | 248 μL | 1.24 mL | 2.4801 mL |
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
g
μL
Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)
Calculation results:
Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid 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 master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
- View current batch:
- Purity: >99.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)