Furaprofen (R803)
(Synonyms: 呋喃洛芬; R803) 目录号 : GC32341
Furaprofen (R803) (R803) 是一种有效的 HCV 复制抑制剂。
Cas No.:67700-30-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Replicon 9-13 cells are plated onto 6-well plates 24 h prior to the treatment. Serial dilutions of Furaprofen are made in a mixture containing 90% of the culture medium, 7.2% 1× PBS, 1.8% methanol, 1% DMSO, 20 μM RBV, and varying concentrations of IFN-α for a fixed-ratio dose-response study. The cells are treated with the designated combinations of Furaprofen (0 to 80 nM concentrations) and IFN-α (0 to 4 IU/mL) plus 20 μM RBV for 72 h; then they are washed with PBS, lysed in SDS loading buffer, and analyzed by Western blotting[1]. |
References: [1]. Huang P, et al. Discovery and characterization of substituted diphenyl heterocyclic compounds as potent and selective inhibitors of hepatitis C virus replication. Antimicrob Agents Chemother. 2008 Apr;52(4):1419-29. | |
Furaprofen (R803) is an effective HCV replication inhibitor. Furaprofen (R803) is substantially more potent against genotype 1a and 1b replicons (EC50, ~30 nM) than against the genotype 2a replicon (EC50, ~1,000 nM).
Furaprofen (R803) is potent and highly specific for HCV replication. The antiviral activity of Furaprofen has been determined by a reporter replicon assay with multiple repeats to be 29.88±8.05 nM, an ~3-fold improvement over the activity of the parent compound, R706. The potency of Furaprofen against the replicon is also confirmed by both Western blotting and TaqMan RT-PCR to be about 37 nM and 54.67±4.11 nM, respectively. To assess the general effect of Furaprofen on cell proliferation, a panel of primary cells and transformed human cell lines are treated with increasing doses of Furaprofen for 48 h, and the effect on cell proliferation is measured by an MTS-based cell viability assay. The the concentration that caused a 50% reduction in cell numbers in the absence of virus infection (CC50) of Furaprofen is found to range from 2 μM to ≥10 μM, depending on the cell type and proliferation status[1].
[1]. Huang P, et al. Discovery and characterization of substituted diphenyl heterocyclic compounds as potent and selective inhibitors of hepatitis C virus replication. Antimicrob Agents Chemother. 2008 Apr;52(4):1419-29.
| Cas No. | 67700-30-5 | SDF | |
| 别名 | 呋喃洛芬; R803 | ||
| Canonical SMILES | OC(C(C1=CC=CC2=C1OC=C2C3=CC=CC=C3)C)=O | ||
| 分子式 | C17H14O3 | 分子量 | 266.29 |
| 溶解度 | DMSO : 250 mg/mL (938.83 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.7553 mL | 18.7765 mL | 37.553 mL |
| 5 mM | 0.7511 mL | 3.7553 mL | 7.5106 mL |
| 10 mM | 0.3755 mL | 1.8777 mL | 3.7553 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Discontinued drugs in 2005: anti-infectives
Expert Opin Investig Drugs 2007 Jan;16(1):1-10.PMID:17155849DOI:10.1517/13543784.16.1.1.
This perspective is the fifth in a series discussing drugs dropped from development in 2005, of which 11 were being developed for infectious diseases. Of these, eight were antivirals and were dropped in Phase II or III: Medivir's alovudine, Ono Pharmaceuticals' aplaviroc hydrochloride and Excite's immunotherapeutic Xcellerate for HIV; Boehringer Ingelheim's ciluprevir, ViroPharma's HCV-086, Isis Pharmaceuticals' antisense oligonucleotide ISIS-14803, Japan Tobacco's JTK-003 and Rigel's R803 for hepatitis C virus. The remaining discontinued anti-infective drugs were an antibacterial vaccine (Vical's anthrax vaccine), an antiseptic (YM Bioscience's Dermofural) and an antifungal formulation (MacroChem's topical econazole). The drugs are grouped by compound class and reasons for their failure are discussed in this article.
Discovery and characterization of substituted diphenyl heterocyclic compounds as potent and selective inhibitors of hepatitis C virus replication
Antimicrob Agents Chemother 2008 Apr;52(4):1419-29.PMID:18227176DOI:10.1128/AAC.00525-07.
A novel small-molecule inhibitor, referred to here as R706, was discovered in a high-throughput screen of chemical libraries against Huh-7-derived replicon cells carrying autonomously replicating subgenomic RNA of hepatitis C virus (HCV). R706 was highly potent in blocking HCV RNA replication as measured by real-time reverse transcription-PCR and Western blotting of R706-treated replicon cells. Structure-activity iterations of the R706 series yielded a lead compound, R803, that was more potent and highly specific for HCV replication, with no significant inhibitory activity against a panel of HCV-related positive-stranded RNA viruses. Furthermore, HCV genotype 1 replicons displayed markedly higher sensitivity to R803 treatment than a genotype 2a-derived replicon. In addition, R803 was tested by a panel of biochemical and cell-based assays for on-target and off-target activities, and the data suggested that the compound had a therapeutic window close to 100-fold, while its exact mechanism of action remained elusive. We found that R803 was more effective than alpha interferon (IFN-alpha) at blocking HCV RNA replication in the replicon model. In combination studies, R803 showed a weak synergistic effect with IFN-alpha/ribavirin but only additive effects with a protease inhibitor and an allosteric inhibitor of RNA-dependent RNA polymerase (20). We conclude that R803 and related heterocyclic compounds constitute a new class of HCV-specific inhibitors that could potentially be developed as a treatment for HCV infection.
Validation of endovascular and open thoracoabdominal aortic aneurysm repair in Ontario health administrative databases
Clin Invest Med 2019 Jun 23;42(2):E19-25.PMID:31228962DOI:10.25011/cim.v42i2.32812.
Purpose: The positive predictive value (PPV) of endovascular and open thoracoabdominal aortic aneurysm (TAAA) repair coding was assessed in Ontario health administrative databases. Methods: Between 1 January 2006 and 31 March 2016, a random sample of 192 patients was identified using Canadian Classification of Health Intervention (CCI) procedure codes and Ontario Health Insurance Plan (OHIP) billing codes from administrative data. Blinded chart reviews were conducted at two cardiovascular centers to assess the level of agreement between the administrative records and the corresponding patients' hospital charts. The PPV was calculated with 95% confidence intervals using hospital charts as the gold standard. Results: The PPV for the single endovascular TAAA repair code, 1ID80GQNRN, was 0.90 (0.78, 0.97). A combination of all nine CCI open TAAA repair codes was performed, with a PPV of 0.62 (0.47, 0.76). The combination of any one of the nine CCI codes AND the single OHIP code for open TAAA repair (R803) rendered a PPV of 0.98 (0.90, 1.00). Conclusions: Endovascular TAAA repair may be identified using a single CCI code (1ID80GQNRN). Open TAAA repair may be identified using a combination of CCI and OHIP codes. Researchers may therefore use administrative data to conduct population-based studies of endovascular and open repair of TAAA.
Intracellular variation of rat intestinal mucin granules localized by monoclonal antibodies
Anat Rec 1991 Aug;230(4):513-8.PMID:1928756DOI:10.1002/ar.1092300410.
Monoclonal antibodies produced against rat small intestinal mucins were utilized to study variability of stored mucin granules within rat ileal goblet cells. Eleven antibody-secreting hybridoma cultures were produced; six of these uniformly labeled stored mucin granules in virtually all goblet cells, suggesting that some antigenic features are common to all granules. The other five stained goblet cells in the rat small intestinal epithelium nonuniformly. R803, R805, and R807 localized within almost all goblet cells but revealed differential labeling of centrally and peripherally located mucin granules. R804 uniformly labeled the mucin granules of most villous goblet cells; some of the crypt goblet cells were uniformly labeled, but the majority were only partially labeled, resulting in a mottled staining pattern. R808 stained only a small portion of crypt goblet cells; there is, however, an increase in both number of goblet cells labeled and in uniformity of staining of the stored granule mass from the base of the crypt to the surface, resulting in uniform labeling of virtually all goblet cells at the villus tip. This study demonstrates for the first time that rat small intestinal mucin granules are immunologically heterogeneous and nonuniformly distributed within the epithelium. Additionally, staining patterns within the stored granule mass suggest that structurally distinct subpopulations of mucin granules may exist within a single goblet cell.
Volume-activated trimethylamine oxide efflux in red blood cells of spiny dogfish (Squalus acanthias)
Am J Physiol Regul Integr Comp Physiol 2001 Sep;281(3):R803-10.PMID:11506995DOI:10.1152/ajpregu.2001.281.3.R803.
The aims of this study were to determine the pathway of swelling-activated trimethylamine oxide (TMAO) efflux and its regulation in spiny dogfish (Squalus acanthias) red blood cells and compare the characteristics of this efflux pathway with the volume-activated osmolyte (taurine) channel present in erythrocytes of fishes. The characteristics of the TMAO efflux pathway were similar to those of the taurine efflux pathway. The swelling-activated effluxes of both TMAO and taurine were significantly inhibited by known anion transport inhibitors (DIDS and niflumic acid) and by the general channel inhibitor quinine. Volume expansion by hypotonicity, ethylene glycol, and diethyl urea activated both TMAO and taurine effluxes similarly. Volume expansion by hypotonicity, ethylene glycol, and diethyl urea also stimulated the activity of tyrosine kinases p72syk and p56lyn, although the stimulations by the latter two treatments were less than by hypotonicity. The volume activations of both TMAO and taurine effluxes were inhibited by tyrosine kinase inhibitors, suggesting that activation of tyrosine kinases may play a role in activating the osmolyte effluxes. These results indicate that the volume-activated TMAO efflux occurs via the organic osmolyte (taurine) channel and may be regulated by the volume activation of tyrosine kinases.