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Daclatasvir (BMS-790052)
Daclatasvir (BMS-790052)
Catalog No.S1482
Synonyms: EBP883
Molecular Weight(MW): 738.88
Daclatasvir (BMS-790052) is a highly selective inhibitor of HCV NS5A with EC50 of 9-50 pM, for a broad range of HCV replicon genotypes and the JFH-1 genotype 2a infectious virus in cell culture. Phase 3.
RMB 1373.65
RMB 2638.39
RMB 7941.93
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Cited by 16 Publications
3 Customer Reviews
The toxicity of BMS-790052 (BMS) and Telaprevir (TPV) was measured by seeding 96-well plates to 70% confluence and exposing the cells to up to 50 &M of compound for 72 hours. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] was added to each well at a final concentration of 500 &g/ml 4 h before dissolving crystals in 100 &l of DMSO and measuring at 550 nm UV wavelengths. The 50% cytotoxic concentration (CC50) was then calculation using the OD550 value and the following formula: log CC50=log concentration of HPP-[(HPP-50)/(HPP-LPP)&log d HPP: highest protective percentage closest to 50% LPP: Lowest protective percentage closest to 50% d: dilution factor
Dr. Julie Sheldon,Dr Esteban Domingo and Dr Celia Perales.
Daclatasvir (BMS-790052) purchased from Selleck.
Huh7.5 cells were infected with JFH-1 (2a) strain. Once the cells reached 80% infectivity they were treated with pMconcentration of BMS790052 for two different time points. Cells were collected in SDS sample loading buffer and probed for NS5A and GAPDH. After 16hrs hyperphosphorylated NS5A disappeared with increasing concentration of the drug. 40hrs of treatment resulted complete disappearance of NS5A. GAPDH is internal control.
Dr. Anita Nag of Florida State University.
Daclatasvir (BMS-790052) purchased from Selleck.
80% infected HCV JFH-1 cells were treated with several concentrations of BMS790052 in pMrange. Cells were fixed after 16hrs and NS5A was probed.Cells treated with BMS790052 shows NS5A present in clusters compared to&an even cytoplasmic distribution in untreated cells.
Dr. Anita Nag of Florida State University.
Daclatasvir (BMS-790052) purchased from Selleck.
Purity & Quality Control
Choose Selective HCV Protease Inhibitors
Biological Activity
Description
Daclatasvir (BMS-790052) is a highly selective inhibitor of HCV NS5A with EC50 of 9-50 pM, for a broad range of HCV replicon genotypes and the JFH-1 genotype 2a infectious virus in cell culture. Phase 3.
First-in-class, highly selective inhibitor of hepatitis C virus (HCV) NS5A with picomolar EC50 values.
9 pM-50 pM(EC50)
BMS-790052 is one of the most potent inhibitors of HCV replication reported so far. The mean EC50 valuses of BMS-790052 are 50 and 9 pM for HCV genotype 1a and 1b replicons, respectively. BMS-790052 displays a therapeutic index (CC50/EC50) of at least 105 and is inactive towards a panel of 10 RNA and DNA viruses, with EC50 higher than 10 μM. This confirms BMS-790052's specificity for HCV.
In Huh7 cells harboring the HCV genotype 1b replicons, BMS-790052 blocks both transient and stable HCV genome replication, with EC50 values raging from 1-15 pM. BMS-0 pM or 1 nM) has been shown to alter the subcellular localization and biochemical fractionation of NS5A.
BMS-790052 inhibits hybrid replicons containing HCV genotype-4 NS5A genes with EC50 of 7-13 pM. Residue 30 of NS5A is an important site for BMS-790052-mediated resistance in the hybrid replicons.
Kinase Assay:
FRET assay for HCV NS5A inhibitors:
The peptide (Ac-Asp-Glu-Asp [EDANS]-Glu-Glu-Abu-[COO] Ala-Ser-Lys [DABCYL]-NH2) contains a fluorescence donor {EDANS, 5-[(2-aminoethyl)amino]naphthalene-1-sulfonic acid} near one end of the peptide and an acceptor {DABCYL, 4-[(4-dimethylamino)phenyl]azo)benzoic acid} near the other end. Intermolecular resonance energy transfer between the donor and the acceptor quenches the fluorescence of the peptide, but as the NS3 protease cleaves the peptide, the products are released from resonance energy transfer quenching. The fluorescence of the donor increases over time as more substrate is cleaved by the NS3 protease. The assay reagent is: 5× luciferase cell culture lysis reagent diluted to 1× with dH2O, NaCl (150 mM), the FRET peptide (20 μM). HCV-Huh-7 cells are placed in a 96-well plate, and allowed to attach overnight (1×104 cells per well). The next day, BMS-790052 is added to the wells and the plate is incubated for 72 hours. The plate is then rinsed with PBS and used for the FRET assay by the addition of 30 μL of the FRET peptide assay reagent (described above) per well. Signals are obtained using the Cytofluor 4000 instrument, which has been set to 340 nm (excitation)/490 nm (emission) automatic mode, for 20 cycles or less, with the plate being read in the kinetic mode. Following FRET, 40 μL of luciferase substrate is added to each well and the luciferase is measured.
Cell Research:
Cell lines: HCV replicon cells (Huh7)
Concentrations: 0.1 pM - 50 μM, dissolved in DMSO (the final concentration of DMSO is 0.5%)
Incubation Time: 72 hours
Method: BMS-790052 is added to 96-well plates containing HCV replicon cells seeded approximately 12 hours before in 200 uL media.The cell plates are tested for replication activity and cytotoxicity after 72 hours of incubation. Cytotoxicity is measured with CellTiter-Blue, after which the media and dye are removed, plates are inverted and the remaining liquid is blotted with paper towels. Replication activity of the HCV genotype 1a cell lines is quantified using Renilla luciferase. 1× Renilla luciferase lysis buffer (30 uL) is added to each well and plates are incubated with gentle shaking for 15 min. Renilla luciferase substrate (40 uL) is then added and the signals are detected using a Top Count luminometer set for light emission quantification. One hundred per cent activity is calculated for each cell line for the DMSO- percentage activity is calculated for each concentration of the inhibitor by dividing the average value for wells containing compound by the average value for wells containing DMSO.(Only for Reference)
References
Solubility (25°C)
(200.3 mM)
(200.3 mM)
* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Information
Molecular Weight
C40H50N8O6
3 years -20&C powder
2 years -80&C in solvent
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Clinical Trial Information
(data from , updated on )
NCT Number
Recruitment
Conditions
Sponsor/Collaborators
Start Date
Recruiting
Hepatitis C
Tanta University
December 2016
Recruiting
Hepatitis C
Kaohsiung Medical University Chung-Ho Memorial Hospital
November 2016
Not yet recruiting
Chronic Hepatitis C
Sang Gyune Kim|Seoul National University Boramae Hospital|Severance Hospital|Inha University Hospital|Korea University|Gachon University Gil Medical Center|Hanyang University Seoul Hospital|Ewha Womans University Mokdong Hospital|Bristol-Myers Squibb|Soonchunhyang University Hospital
September 2016
Not yet recruiting
Hepatitis c
Tainan Municipal Hospital
Not yet recruiting
Hepatitis C
Zagazig University|Cairo University
Recruiting
Hepatitis C, Chronic|Hepatocellular Carcinoma
National Hepatology & Tropical Medicine Research Institute|Cairo University
March 2016
Tech Support
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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& Copyright 2013 Selleck Chemicals. All Rights Reserved.Daclatasvir dihydrochloride的生物活性
BMS-790052 is a highly selective inhibitor of HCV NS5A with EC50 of 9-50 pM, for a broad range of HCV replicon genotypes and the JFH-1 genotype 2a infectious virus in cell culture.
IC50 Value: 9-50 pM
Target: HCV NS5A
BMS-790052 has broad genotype coverage and exhibits picomolar in vitro potency against genotypes 1a (EC50 50pm) and 1b (EC50 9pm). BMS-790052 produces a robust decline in HCV RNA (-3.6 logs after 48 hours from a single 100 mg) dosefollowing a single dose in patients chronically infected with HCV genotype 1.
参考CoA中推荐的条件进行储存。
C??H??Cl?N?O?
溶剂/溶解度
10 mM in DMSO
BMS-790052 is the most potent hepatitis C virus (HCV) inhibitor reported to date, with 50% effective concentrations (EC(50)s) of & or = 50 pM against genotype 1 replicons. This exceptional potency translated to rapid viral load declines in a phase I clinical study. By targeting NS5A, BMS-790052 is distinct from most HCV inhibitors in clinical evaluation. As an initial step toward correlating in vitro and in vivo resistances, multiple cell lines and selective pressures were used to identify BMS-790052-resistant variants in genotype 1 replicons. Similarities and differences were observed between genotypes 1a and 1b. For genotype 1b, L31F/V, P32L, and Y93H/N were identified as primary resistance mutations. L23F, R30Q, and P58S acted as secondary resistance substitutions, enhancing the resistance of primary mutations but themselves not conferring resistance....
BACKGROUND: Hepatitis C virus (HCV) of genotype 1b is the most prevalent worldwide, and the least responsive to interferon-based treatments. A combination therapy with two direct-acting antivirals has shown promising results in patients with HCV-1b, but the prevalence of drug-resistant variants before treatment is not known in the Japanese population. OBJECTIVES: To detect HCV variants resistant to NS3 protease inhibitors or the NS5A inhibitor (BMS-790052) in hepatitis patients infected with HCV-1b. STUDY DESIGN: Drug-resistant mutations were determined in the 362 hepatitis patients infected with HCV-1b who had not received direct-acting antivirals before. RESULTS: Amino-acid substitutions resistant to NS3 inhibitors (V36A, T54S, Q80H and D168E) were detected in 15 of the 307 (4.9%) patients, who had been examined, and T54S (3.3%) predominated over V36A (0.3%), Q80R (0.7%) and D168E (0.7%) in them. Amino-acid substitutions resistant to BMS-790052 (L31M and/or Y93H) were detected in 33 of the 294 (11.2%) patients, and Y93H (8.2%) predominated over L31M (2.7%). One of the 239 (0.4%) patients, who had been examined for amino-acid substitutions in both NS3 and NS5A regions, possessed HCV-1b variants resistant to NS3 inhibitors (T54S) and BMS-790052 (L31M)...
A liquid-liquid extraction (LLE) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) methods have been developed and validated for the quantification of BMS-790052 (daclastasvir) in human plasma and urine. The samples were extracted with methyl-t-butyl ether (MTBE) before analyzing by an API 4000 mass spectrometer which was operated in a multiple reaction monitoring (MRM) mode for detection of positively charged ions of BMS-790052 and its internal standard, 13C??-BMS-790052. The standard curves ranged from 0.050 to 50.0 ng/mL for BMS-790052 in human plasma, and 1.00-1000 ng/mL in human urine. The intra-assay precision (%CV), based on four levels of analytical QCs (low, geometric mean, mid and high), was within 8.6%; inter-assay precision (%CV) was within 6.7% for both plasma and urine methods, and the mean assay accuracy (%Dev) was within &3.0% for both plasma and urine methods. The ruggedness of this accurate, precise, and selective LLE-LC-MS/MS method has been demonstrated in the successful analysis of several thousand clinical study samples.
The influence of naturally occurring polymorphisms on the potency of the HCV nonstructural protein 5A (NS5A) replication complex inhibitor, BMS-790052, was investigated by evaluating hybrid replicons in which the entire NS5A coding region of genotype (GT) la and 1b laboratory (lab) strains (H77c and Con1) were replaced with the corresponding regions of specimens collected from 10 GT-1a- and 6 GT-1b-infected subjects. For baseline (BL) specimens, with no previously observed resistance variants identified by population sequencing, the median 50% effective concentration (EC(50) ) values for BMS-790052 were similar for the clinically derived and lab strains. A Q30R variant was observed at viral breakthrough (VBT) in one of the GT-1a-infected subjects. Because the lowest plasma exposure of BMS-790052 observed in this subject was 117 nM and the median 50% effective concentration value for a GT-1a H77c replicon containing a Q30R substitution is ~7 nM, a rigorous investigation was initiated to determine the basis for resistance. Three approaches were used: (1) replacement of the entire H77c NS5A or (2) replacement of the N-terminal region of NS5A, with sequence from BL and day 14, and (3) substitution of specific amino acids. A BL polymorphism (E62D) did not contribute resistance to BMS-790052; however, the linked variant, Q30R-E62D, conferred high-level resistance in vitro and is likely responsible for VBT in vivo. CONCLUSION: Our data show that a BL polymorphism with minimal effect on the anti-HCV effect of BMS-790052 can affect the emergence of resistance and significantly affect clinical outcome. This work establishes a clear, systematic approach to monitor resistance to NS5A inhibitors in the clinic.
The antiviral profile of BMS-790052, a potent hepatitis C virus (HCV) replication complex inhibitor targeting nonstructural protein NS5A, is well characterized for HCV genotype-1. Here, we report that BMS-790052 inhibits hybrid replicons containing HCV genotype-4 NS5A genes with 50% effective concentrations (EC(50)s) ranging from 7 to 13 pM. NS5A residue 30 was an important site for BMS-790052-selected resistance in the hybrid replicons. Our results support the potential of BMS-790052 as a valuable component of combination therapy for HCV genotype-4 chronic infection.免费电话：400-668-6834 | 技术支持：400-168-6834 | 邮箱：
Daclatasvir (BMS-790052)
Daclatasvir (BMS-790052)
Catalog No.S1482
Synonyms: EBP883
Molecular Weight(MW): 738.88
Daclatasvir (BMS-790052)是一种高度选择性的HCV NS5A抑制剂，EC50为9-50 pM，在细胞培养中，作用于多种HCV复制基因型和JFH-1基因型2a的感染性病毒。Phase 3。
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客户使用该产品发表的文献16篇：
客户使用该产品的3个实验数据：
The toxicity of BMS-790052 (BMS) and Telaprevir (TPV) was measured by seeding 96-well plates to 70% confluence and exposing the cells to up to 50 &M of compound for 72 hours. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] was added to each well at a final concentration of 500 &g/ml 4 h before dissolving crystals in 100 &l of DMSO and measuring at 550 nm UV wavelengths. The 50% cytotoxic concentration (CC50) was then calculation using the OD550 value and the following formula: log CC50=log concentration of HPP-[(HPP-50)/(HPP-LPP)&log d HPP: highest protective percentage closest to 50% LPP: Lowest protective percentage closest to 50% d: dilution factor
Dr. Julie Sheldon,Dr Esteban Domingo and Dr Celia Perales.
Daclatasvir (BMS-790052) purchased from Selleck.
Huh7.5 cells were infected with JFH-1 (2a) strain. Once the cells reached 80% infectivity they were treated with pMconcentration of BMS790052 for two different time points. Cells were collected in SDS sample loading buffer and probed for NS5A and GAPDH. After 16hrs hyperphosphorylated NS5A disappeared with increasing concentration of the drug. 40hrs of treatment resulted complete disappearance of NS5A. GAPDH is internal control.
Dr. Anita Nag of Florida State University.
Daclatasvir (BMS-790052) purchased from Selleck.
80% infected HCV JFH-1 cells were treated with several concentrations of BMS790052 in pMrange. Cells were fixed after 16hrs and NS5A was probed.Cells treated with BMS790052 shows NS5A present in clusters compared to&an even cytoplasmic distribution in untreated cells.
Dr. Anita Nag of Florida State University.
Daclatasvir (BMS-790052) purchased from Selleck.
产品安全说明书
HCV Protease抑制剂选择性比较
Daclatasvir (BMS-790052)是一种高度选择性的HCV NS5A抑制剂，EC50为9-50 pM，在细胞培养中，作用于多种HCV复制基因型和JFH-1基因型2a的感染性病毒。Phase 3。
BMS-790052是一流的高选择性C型肝炎病毒(HCV) NS5A抑制剂， EC50为皮摩尔级。
9 pM-50 pM(EC50)
BMS-790052是到目前为止报道的最有效的HCV复制抑制剂之一,作用于HCV基因型1a和1b复制子时EC50分别为50和9 pM。 BMS-790052治疗指数(CC50/EC50)为105以上，对一组10种RNA和DNA病毒没有作用效果, EC50大于10 μM, BMS-790052只针对HCV有效。 BMS-790052作用于含HCV基因型1b复制子的Huh7细胞, BMS-790052抑制短暂和稳定的HCV染色体复制, EC50为1-15 pM。BMS-0 pM或1 nM)改变NS5A的亚细胞定位和生化结构。 BMS-790052抑制含HCV基因型-4 NS5A基因的杂合复制子，EC50为7-13 pM。杂合复制子中的NS5A残基30是BMS-790052选择耐抗性的一个重要位点。
推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)
激酶实验：
针对HCV NS5A抑制剂的FRET实验 :
肽段 (Ac-Asp-Glu-Asp [EDANS]-Glu-Glu-Abu-[COO] Ala-Ser-Lys [DABCYL]-NH2)含荧光供体{EDANS, 5-[(2-氨乙基)氨基]萘-1-磺酸} ，位于肽段一端；受体 {DABCYL, 4-[4-(二甲基氨基)苯偶氮]苯甲酸}，位于肽段另一端。通过在供体和受体之间分子能量共振转移使肽段荧光淬灭，NS3蛋白酶使肽段断裂，共振能量转移淬灭使产物释放，供体的荧光随着底物被NS3蛋白酶降解的时间而增强。反应所用试剂如下：5×荧光素酶细胞培养液用dH2O稀释到1×,NaCl (150 mM), FRET肽(20 μM)。HCV-Huh-7细胞按每孔1×104个接种在96孔板上，粘附过夜。 第二天, BMS-790052加到孔中，温育72小时。用PBS冲洗板，每孔加入30 μL FRET肽实验试剂进行FRET实验。使用Cytofluor 4000仪测定吸光值。随后，40 μL荧光素酶底物加到每孔中，测定荧光值。
细胞实验：
Cell lines: HCV复制子细胞(Huh7)
Concentrations: 0.1 pM-50 uM, 溶于DMSO，最终DMSO浓度为0.5%
Incubation Time: 72小时
Method: 细胞接种在96孔板上的200uL培养基中，12小时后，BMS-790052加到含HCV复制子的96孔板上。温育72小时，测定复制活性和细胞毒性。使用CellTiter-Blue测定细胞毒性。随后，移除培养基和染料，使板倒转，残留的液体用纸巾吸干，使用Renilla荧光素酶测定HCV 基因型1a细胞系的复制活性。1×Renilla荧光素酶溶解buffer (30 uL)加到每孔中，温和震荡15分钟。加入Renilla荧光素酶底物(40 uL)， 使用Top Count光度计测定信号。(Only for Reference)
溶解度 (25°C)
(200.3 mM)
(200.3 mM)
* &1 mg/ml 指产品微溶或不溶
* 溶解度检测是由Selleck技术部门检测的，可能会和文献中提供的溶解度有所差异，这是由于生产工艺和批次不同产生的正常现象。
C40H50N8O6
3 years -20&C powder
2 years -80&C in solvent
摩尔浓度计算器
本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系，公式为:
质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量
摩尔浓度计算公式
*在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。
稀释计算器
用本工具协助配置特定浓度的溶液，使用的计算公式为：
开始浓度 x 开始体积 = 最终浓度 x 最终体积
稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出
在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。.
连续稀释计算器方程
分子量计算器
通过输入化合物的化学式来计算其分子量：
总分子量：g/mol
注：化学分子式大小写敏感。C10H16N2O2 c10h16n2o2
摩尔浓度计算器
临床试验信息
(data from , updated on )
NCT Number
Recruitment
Conditions
Sponsor/Collaborators
Start Date
Recruiting
Hepatitis C
Tanta University
December 2016
Recruiting
Hepatitis C
Kaohsiung Medical University Chung-Ho Memorial Hospital
November 2016
Not yet recruiting
Chronic Hepatitis C
Sang Gyune Kim|Seoul National University Boramae Hospital|Severance Hospital|Inha University Hospital|Korea University|Gachon University Gil Medical Center|Hanyang University Seoul Hospital|Ewha Womans University Mokdong Hospital|Bristol-Myers Squibb|Soonchunhyang University Hospital
September 2016
Not yet recruiting
Hepatitis c
Tainan Municipal Hospital
Not yet recruiting
Hepatitis C
Zagazig University|Cairo University
Recruiting
Hepatitis C, Chronic|Hepatocellular Carcinoma
National Hepatology & Tropical Medicine Research Institute|Cairo University
March 2016
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