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5mg |
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10mg |
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25mg |
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50mg |
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100mg |
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250mg |
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Purity: ≥98%
RN-18 is an HIV-1 Vif inhibitor. RN-18 antagonizes Vif function and inhibits HIV-1 replication only in the presence of A3G. RN-18 increases cellular A3G levels in a Vif-dependent manner and increases A3G incorporation into virions without inhibiting general proteasome-mediated protein degradation. RN-18 enhances Vif degradation only in the presence of A3G, reduces viral infectivity by increasing A3G incorporation into virions and enhances cytidine deamination of the viral genome.
Targets |
nonpermissive H9 cell( IC50=6 μM )
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ln Vitro |
Strong antiviral activity is shown by RN-18 and RN-19 in nonpermissive H9 and CEM cells, but not in MT4 or CEM-SS cells, indicating that the antiviral action was Vif specific. Between the two compounds, RN-18 exhibits higher specificity (IC50>100 μM in MT4 cells) and potency (IC50=4.5 μM in CEM cells[1]. Reverse transcriptase activity in the nonpermissive H9 and CEM cells is significantly and dose-dependently reduced in the presence of the inhibitor, RN-18. While RN-18 does not show antiviral activity in the original CEM-SS cell line, it does show antiviral activity in CEM-SS modified to stably express A3G. If A3G is present, only then does RN-18 counteract Vif function and prevent HIV-1 replication. RN-18 does not impede the general proteasome-mediated protein degradation process, but it does raise cellular A3G levels in a Vif-dependent manner and increase A3G incorporation into virions. Only in the presence of A3G does RN-18 increase Vif degradation; it also increases cytidine deamination of the viral genome, decreases viral infectivity by increasing A3G incorporation into virions[2].
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References |
Molecular Formula |
C20H16N2O4S
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Molecular Weight |
380.418
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Exact Mass |
380.0831
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Elemental Analysis |
C, 63.15; H, 4.24; N, 7.36; O, 16.82; S, 8.43
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CAS # |
431980-38-0
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Related CAS # |
431980-38-0
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Appearance |
Solid powder
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SMILES |
O=C(NC1=CC=CC=C1OC)C2=CC=CC=C2SC3=CC=C([N+]([O-])=O)C=C3
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InChi Key |
JKNUDHUHXMELIJ-UHFFFAOYSA-N
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InChi Code |
InChI=1S/C20H16N2O4S/c1-26-18-8-4-3-7-17(18)21-20(23)16-6-2-5-9-19(16)27-15-12-10-14(11-13-15)22(24)25/h2-13H,1H3,(H,21,23)
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Chemical Name |
N-(2-methoxyphenyl)-2-[(4-nitrophenyl)thio]-benzamide
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Synonyms |
RN-18; RN 18; RN18.
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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 |
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) |
DMSO : ~100 mg/mL (~262.87 mM)
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Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 :Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400  (Please use freshly prepared in vivo formulations for optimal results.) |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 2.6287 mL | 13.1434 mL | 26.2867 mL | |
5 mM | 0.5257 mL | 2.6287 mL | 5.2573 mL | |
10 mM | 0.2629 mL | 1.3143 mL | 2.6287 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.
Vif antagonists inhibit HIV-1 replication in nonpermissive H9 cells but not in permissive MT4 cells.[1].SAR and Lead Optimization of an HIV-1 Vif-APOBEC3G Axis Inhibitor. ACS Med Chem Lett. 2012 Jun 14;3(6):465-469. td> |
Vif antagonist small molecules enhance A3G levels and reduce Vif expression. [1].SAR and Lead Optimization of an HIV-1 Vif-APOBEC3G Axis Inhibitor. ACS Med Chem Lett. 2012 Jun 14;3(6):465-469. td> |