(R)-Flurbiprofen
CAS No. 51543-40-9
(R)-Flurbiprofen( E7869 | Tarenflurbil | MPC7869 )
Catalog No. M14791 CAS No. 51543-40-9
A non-steroidal anti-inflammatory drug (NSAID); primarily indicated as a pre-operative anti-miotic as well as orally for arthritis or dental pain; cyclooxygenase (COX) inhibitor.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
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| 200MG | Get Quote | In Stock |
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| 500MG | Get Quote | In Stock |
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| 1G | Get Quote | In Stock |
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Biological Information
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Product Name(R)-Flurbiprofen
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NoteResearch use only, not for human use.
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Brief DescriptionA non-steroidal anti-inflammatory drug (NSAID); primarily indicated as a pre-operative anti-miotic as well as orally for arthritis or dental pain; cyclooxygenase (COX) inhibitor.
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DescriptionA non-steroidal anti-inflammatory drug (NSAID); primarily indicated as a pre-operative anti-miotic as well as orally for arthritis or dental pain; cyclooxygenase (COX) inhibitor.Pain Approved(In Vitro):Tarenflurbil ((R)-Flurbiprofen) can significantly reduce Aβ secretion, but at the same time, increases the level of intracellular Aβ. The binding between [3H]9-cis-RA and RXRα is competitively inhibited by both unlabeled (R)-Flurbiprofen and 9-cis-RA. (R)-Flurbiprofen can interfere with the interaction between RXRα and 9-cis-retinoid acid (9-cis-RA), and that 9-cis-RA decreases Tarenflurbil ((R)-Flurbiprofen)’s reduction of Aβ secretion. Tarenflurbil ((R)-Flurbiprofen) treatment significantly increases the levels of intracellular Aβ species. The well characterized, nonsteroidal anti-inflammatory drug (nonsteroidal anti-inflammatory drug), Tarenflurbil ((R)-Flurbiprofen) affects only Aβ and not Notch β formation, indicating that second generation GSMs and nonsteroidal anti-inflammatory drug-based GSMs have different modes of action regarding Notch processing. (In Vivo):Effects of the early and late onset of treatment with Tarenflurbil ((R)-Flurbiprofen) are assessed in C57BL6/J mice that develop a non-remitting form of the disease, and in SJL mice that develop a relapsing-remitting (RR)-EAE. Tarenflurbil ((R)-Flurbiprofen) completely prevents the development of clinical EAE scores in C57BL6/J mice when the treatment is started within 3 days after immunization. This regimen is referred to as preventive treatment. The effect is dose-dependent, and the minimum daily dose for complete prevention is 5 mg/kg/day. Effects of Tarenflurbil ((R)-Flurbiprofen) are comparable to those of Fingolimod (FTY720, 0.5 mg/kg/day), which is used as the positive control. Tarenflurbil ((R)-Flurbiprofen) also significantly reduces clinical EAE scores in C57BL6/J mice when treatment is started shortly before onset of clinical manifestations, referred to as semi-therapeutic (10 mg/kg/day) and reduces clinical scores when the treatment is initiated after full development of the disease on day 13 (5 mg/g/day).
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In VitroTarenflurbil ((R)-Flurbiprofen) can significantly reduce Aβ secretion, but at the same time, increases the level of intracellular Aβ. The binding between [3H]9-cis-RA and RXRα is competitively inhibited by both unlabeled (R)-Flurbiprofen and 9-cis-RA. (R)-Flurbiprofen can interfere with the interaction between RXRα and 9-cis-retinoid acid (9-cis-RA), and that 9-cis-RA decreases Tarenflurbil ((R)-Flurbiprofen)’s reduction of Aβ secretion. Tarenflurbil ((R)-Flurbiprofen) treatment significantly increases the levels of intracellular Aβ species. The well characterized, nonsteroidal anti-inflammatory drug (nonsteroidal anti-inflammatory drug), Tarenflurbil ((R)-Flurbiprofen) affects only Aβ and not Notch β formation, indicating that second generation GSMs and nonsteroidal anti-inflammatory drug-based GSMs have different modes of action regarding Notch processing. They are for reference only.
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In VivoEffects of the early and late onset of treatment with Tarenflurbil ((R)-Flurbiprofen) are assessed in C57BL6/J mice that develop a non-remitting form of the disease, and in SJL mice that develop a relapsing-remitting (RR)-EAE. Tarenflurbil ((R)-Flurbiprofen) completely prevents the development of clinical EAE scores in C57BL6/J mice when the treatment is started within 3 days after immunization. This regimen is referred to as preventive treatment. The effect is dose-dependent, and the minimum daily dose for complete prevention is 5 mg/kg/day. Effects of Tarenflurbil ((R)-Flurbiprofen) are comparable to those of Fingolimod (FTY720, 0.5 mg/kg/day), which is used as the positive control. Tarenflurbil ((R)-Flurbiprofen) also significantly reduces clinical EAE scores in C57BL6/J mice when treatment is started shortly before onset of clinical manifestations, referred to as semi-therapeutic (10 mg/kg/day) and reduces clinical scores when the treatment is initiated after full development of the disease on day 13 (5 mg/g/day).
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SynonymsE7869 | Tarenflurbil | MPC7869
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PathwayChromatin/Epigenetic
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TargetCOX
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RecptorCOX
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Research AreaNeurological Disease
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IndicationPain
Chemical Information
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CAS Number51543-40-9
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Formula Weight244.2609
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Molecular FormulaC15H13FO2
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Purity>98% (HPLC)
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Solubility10 mM in DMSO
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SMILESC[C@H](C1=CC=C(C2=CC=CC=C2)C(F)=C1)C(O)=O
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Chemical Name[1,1'-Biphenyl]-4-acetic acid, 2-fluoro-α-methyl-, (αR)-
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1. Chalmers IM, et al. Ann Rheum Dis. 1972 Jul;31(4):319-24.
2. King JG Jr, et al. Oncogene. 2001 Oct 18;20(47):6864-70.
3. Peretto I, et al. J Med Chem. 2005 Sep 8;48(18):5705-20.
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