HIV reverse transcriptase (RT) and HBV DNA polymerase (nucleoside reverse transcriptase inhibitor, NRTI);
- Against HIV-1 in human PBMCs, Emtricitabine (BW1592) had an EC50 of 0.01 μM (HIV-1IIIB strain) and 0.02 μM (HIV-1BaL strain) [1]
- Against HBV in HepG2.2.15 cells (HBV-expressing), Emtricitabine (BW1592) inhibited HBV DNA synthesis with an IC50 of 0.1 μM [1]

恩曲他滨对 HIV-1 临床分离株以及 HIV-1 和 HIV-2 实验室毒株表现出体外功效。 EC50（或 50% 有效浓度）根据所使用的细胞系和病毒分离株在 0.002 至 1.5 μmol/L 之间变化。当与去羟肌苷或扎西他滨配对时，恩曲他滨在体外具有活性，并在体外与司他夫定和齐多夫定产生协同作用[1]。

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1. 抗HIV与HBV体外活性：
- 在HIV-1感染的人PBMCs中，Emtricitabine (BW1592)（0.01–0.1 μM）呈剂量依赖性降低HIV-1 p24抗原：0.05 μM时降低90% ± 4%，0.1 μM时抑制率>95% [1]
- 在HepG2.2.15细胞中，Emtricitabine（0.05–0.5 μM）降低HBV DNA水平：0.1 μM时降低50% ± 3%，0.5 μM时降低80% ± 4%（实时PCR检测）[1]
2. 抑制神经祖细胞（NPC）增殖：
- 在小鼠胚胎NPCs（神经球培养）中，Emtricitabine (BW1592)（10 μM）单独处理降低神经球形成率22% ± 3%；与Tenofovir DF（10 μM）和Raltegravir（1 μM）联用时，形成率降低55% ± 5%（Nestin免疫染色）[2]
- NPC增殖（EdU掺入实验）：单独处理降低18% ± 2%，三联处理降低48% ± 4% [2]
3. 影响内皮细胞功能：
- 在人脐静脉内皮细胞（HUVECs）中，Emtricitabine (BW1592)（5–20 μM）剂量依赖性升高PARP活性（20 μM时升高2.1倍），降低一氧化氮（NO）生成（20 μM时降低35% ± 4%）[4]
- 20 μM浓度下，Emtricitabine不影响HUVEC活力（MTT法，活力较对照组>90%）[4]

恩曲他滨用于与生殖和发育相关的毒性研究。妊娠动物口服剂量高达 1000 mg/kg/天，每日一次的每日曲线下面积 (AUC0→24) 约为 60 至 120 倍（小鼠至兔子），大于人类推荐量（200 毫克）。在小鼠生育力研究中，恩曲他滨对精子数量、早期胚胎发育或生育力没有影响。对小鼠和兔子的胚胎胎儿毒性的研究并未显示异常发生率较高。在小鼠产前或产后试验中，恩曲他滨对 F1 后代的发育或生育力没有影响。根据这些发现，恩曲他滨具有良好的临床前生殖安全性[2]。

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1. 动物模型抗病毒效果：
- 在HIV-1感染的SCID小鼠（重建人PBMC）中，口服Emtricitabine (BW1592)（20 mg/kg/天）14天，血浆HIV-1 RNA较对照组降低2.3 log10拷贝/mL [1]
- 在HBV转基因小鼠中，口服Emtricitabine（30 mg/kg/天）21天，肝脏HBV DNA降低65% ± 5%（Southern blot检测）[1]
2. 对胎鼠神经祖细胞的影响：
- 孕C57BL/6小鼠从妊娠第10天至出生后第7天口服Emtricitabine (BW1592)（30 mg/kg/天）：
- 新生后代脑NPC增殖（Ki67染色）较对照组降低20% ± 3% [2]
- 无显著胎鼠死亡或神经组织学损伤 [2]
3. 啮齿类动物生殖毒性：
- CD-1小鼠（口服Emtricitabine (BW1592) 50、150、500 mg/kg/天，妊娠第6–15天）：
- 胚胎吸收率无升高；500 mg/kg组胎仔体重降低8% ± 2% [3]
- 新西兰白兔（口服10、30、100 mg/kg/天，妊娠第6–18天）：
- 无致畸性；100 mg/kg组胎仔体重降低10% ± 3% [3]

试剂制备：重组HIV-1 RT重悬于实验缓冲液（50 mM Tris-HCl，pH 7.8，7.5 mM MgCl₂，50 mM KCl）；Emtricitabine (BW1592) 用DMSO配制为系列浓度（0.001–1 μM）；生物素标记的poly(rC)-oligo(dG)（底物）和地高辛标记的dGTP用实验缓冲液稀释 [1]
- 实验流程：50 μL反应体系含HIV-1 RT（0.4 μg）、底物（80 ng）、dGTP（8 μM）及不同浓度Emtricitabine，37°C孵育45分钟；加入20 μL 0.6 M EDTA终止反应 [1]
- 检测与分析：反应液转移至链霉亲和素包被的96孔板，洗涤后加入抗地高辛-HRP偶联物；TMB底物显色，检测450 nm吸光度；通过量效曲线拟合计算EC50 [1]

1. 神经祖细胞（NPC）实验：
- 细胞分离与培养：从E14.5小鼠胚胎前脑分离NPCs，用神经球培养基（DMEM/F12 + 20 ng/mL EGF + 20 ng/mL bFGF + 2% B27）在37°C、5% CO₂条件下培养 [2]
- 药物处理：NPCs（1×10⁴细胞/孔）接种于96孔板，用Emtricitabine (BW1592)（1、5、10 μM）单独或与Tenofovir DF（10 μM）+ Raltegravir（1 μM）处理72小时 [2]
- 检测方法：
- 神经球形成：倒置显微镜下计数，形成率=（实验组球数/对照组球数）×100% [2]
- 增殖检测：EdU掺入实验（荧光染色，流式细胞术定量）[2]
2. HUVEC内皮细胞实验：
- 细胞培养：HUVECs用含10% FBS的EGM-2培养基在37°C、5% CO₂条件下培养 [4]
- 药物处理：融合的HUVECs用Emtricitabine (BW1592)（5、10、20 μM）处理24小时，未处理细胞作为对照 [4]
- 检测方法：
- PARP活性：比色法试剂盒检测（405 nm吸光度）[4]
- NO生成：Griess试剂检测（540 nm吸光度）[4]
- 细胞活力：MTT法检测（570 nm吸光度）[4]
3. HIV-1感染PBMC实验：
- 细胞制备：密度梯度离心法分离人PBMCs，用5 μg/mL PHA + 10 U/mL IL-2激活3天 [1]
- 感染与处理：活化PBMCs（1×10⁶细胞/mL）感染HIV-1IIIB（MOI=0.01）2小时后，用Emtricitabine（0.005–0.1 μM）处理 [1]
- 病毒检测：ELISA检测上清液中HIV-1 p24抗原；实时RT-PCR定量病毒RNA [1]

Oral
Mouse

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1. Pregnant mouse neural development model :
- Animals and grouping: Pregnant C57BL/6 mice (n=7/group) were randomly divided into:
- Control group: Oral gavage of 0.5% carboxymethyl cellulose (CMC) once daily (gestational day 10 to postnatal day 7) [2]
- Emtricitabine group: Oral gavage of Emtricitabine (BW1592) (30 mg/kg/day, dissolved in 0.5% CMC) once daily [2]
- Triple combination group: Oral gavage of Emtricitabine (30 mg/kg/day) + Tenofovir DF (30 mg/kg/day) + Raltegravir (10 mg/kg/day) once daily [2]
- Detection: On postnatal day 7, mice were euthanized; brains were fixed in 4% paraformaldehyde. Ki67 immunostaining was used to quantify NPC proliferation [2]
2. Rodent reproductive toxicity model :
- Mouse experiment:
- Animals: CD-1 mice (female: 8–10 weeks old; male: 10–12 weeks old) [3]
- Grouping and treatment: Female mice were orally administered Emtricitabine (BW1592) (50, 150, 500 mg/kg/day) from gestational day 6 to 15; males were dosed for 30 days before mating [3]
- Detection: On gestational day 18, females were euthanized; embryo resorption rate, fetal body weight, and external malformations were recorded [3]
- Rabbit experiment:
- Animals: New Zealand White rabbits (female: 6–8 months old) [3]
- Grouping and treatment: Females were orally administered Emtricitabine (BW1592) (10, 30, 100 mg/kg/day) from gestational day 6 to 18 [3]
- Detection: On gestational day 29, females were euthanized; fetal viability, body weight, and organ malformations were evaluated [3]
3. HIV-1 SCID mouse model :
- Animals and grouping: SCID mice (6–8 weeks old) were intraperitoneally injected with human PBMCs (5×10⁶ cells/mouse) and infected with HIV-1IIIB (1×10⁴ TCID50/mouse) 3 days later [1]
- Treatment: Infected mice were orally administered Emtricitabine (BW1592) (20 mg/kg/day, dissolved in normal saline) once daily for 14 days; control mice received normal saline [1]
- Detection: Plasma HIV-1 RNA was quantified by real-time RT-PCR every 3 days [1]

Absorption, Distribution and Excretion
The peak plasma concentration (Cmax) of emtricitabine is 1.8 ± 0.7 µg/mL, the time to peak concentration (Tmax) is 1–2 hours, and the AUC is 10 ± 3.1 µg/mL. The bioavailability of emtricitabine capsules is 93%, and the bioavailability of oral solution is 75%. Co-administration with food reduces Cmax by 29%. [L9019] 86% of emtricitabine is excreted in the urine and 14% in the feces. 13% of the dose is excreted in the urine as metabolites; 9% exists as the 3'-sulfoxide diastereomer and 4% exists as the 2'-O-glucuronide. The apparent central volume of distribution is 42.3 L, and the peripheral volume of distribution is 55.4 L. The apparent elimination rate of emtricitabine is 15.1 L/hour. The elimination rate is closely related to creatinine clearance.
Embrytabine is rapidly and extensively absorbed after oral administration, with peak plasma concentrations occurring 1 to 2 hours after dosing. In 20 HIV-infected patients, after multiple oral administrations of emtricitabine, the steady-state peak plasma concentration (Cmax) (mean ± standard deviation) was 1.8 ± 0.7 μg/mL, and the area under the plasma concentration-time curve (AUC) over the 24-hour dosing interval was 10.0 ± 3.1 h/μg/mL. The mean steady-state trough plasma concentration 24 hours after dosing was 0.09 μg/mL. The mean absolute bioavailability of emtricitabine was 93%.
In vitro, emtricitabine binds to human plasma proteins <4%, and this binding is concentration-independent within the concentration range of 0.02 to 200 μg/mL. At peak plasma concentrations, the mean ratio of plasma to blood drug concentration was approximately 1.0, and the mean ratio of semen to plasma drug concentration was approximately 4.0.
Time to peak concentration: 1 to 2 hours after dosing. Emtricitabine is distributed in human milk at low concentrations. For more complete data on the absorption, distribution, and excretion of emtricitabine (6 components), please visit the HSDB record page. Metabolism/Metabolites Approximately 86% of emtricitabine is not metabolized. Approximately 9% of the dose is metabolized to the 3'-sulfoxide diastereomer, 4% to 2'-O-glucuronide, and a small amount is converted to 5-fluorocytosine. Biotransformation of emtricitabine includes partial oxidation of thiols to form the 3'-sulfoxide diastereomer (approximately 9% of the dose) and conjugation with glucuronic acid to form 2'-O-glucuronide (approximately 4% of the dose). No other metabolites have been identified. Emtricitabine is not metabolized by hepatic enzymes. Biological Half-Life The half-life of emtricitabine is approximately 10 hours. The plasma half-life of emtricitabine is approximately 10 hours.

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Absorption: The oral bioavailability of emtricitabine (BW1592) in humans (fasting) is 93% ± 4% and in rats is 88% ± 3%. 1.5 hours after oral administration of 200 mg, the peak plasma concentration (Cmax) was 1.6 ± 0.2 μg/mL [1]
- Distribution: The volume of distribution (Vd) in the human body was 1.4 ± 0.2 L/kg; it was distributed in cerebrospinal fluid (CSF/plasma ratio = 0.3 ± 0.05) and vaginal tissue (tissue/plasma ratio = 2.1 ± 0.2) [1]
- Metabolism: Emtricitabine (BW1592) is metabolized very little in the liver (<5% of the dose); the major metabolite is inactive (emtricitabine glucuronide) [1]
- Excretion: The elimination half-life (t1/2) in the human body was 10.5 ± 1.2 hours. Within 72 hours, 86% ± 5% of the dose was excreted in the urine (70% as the original drug and 16% as glucuronide metabolites) [1]
- Plasma protein binding rate: The plasma protein binding rate of emtricitabine (BW1592) in human plasma was 4% ± 1%, and the plasma protein binding rate in rat plasma was 5% ± 1% [1]

Hepatotoxicity
Currently, there is insufficient evidence to suggest that emtricitabine has direct hepatotoxicity, nor has it been found to be directly associated with lactic acidosis with steatosis and liver failure. However, patients with chronic hepatitis B may experience acute exacerbations of primary hepatitis during emtricitabine treatment. These exacerbations can occur at the beginning of treatment (treatment-induced exacerbation), when antiviral resistance develops (breakthrough exacerbation), or when treatment is abruptly discontinued (discontinuation-induced exacerbation). Treatment-induced exacerbations occur in approximately 5% to 10% of cases, are usually transient and asymptomatic, and rarely require dose adjustment or discontinuation. In contrast, discontinuation-induced exacerbations occur in approximately 15% to 30% of cases, but can be symptomatic and severe, and in rare cases (approximately 1%) can lead to acute liver failure, death, or the need for emergency liver transplantation. Patients who develop resistance to emtricitabine often experience disease relapse after the appearance of HBV mutant strains and elevated HBV DNA levels; this relapse may initially be severe, accompanied by symptoms and jaundice.

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Impact of Pregnancy and Lactation
◉ Overview of Lactational Use
The use of emtricitabine during lactation is well-studied and is sometimes used to treat HIV-positive mothers who are breastfeeding. Achieving and maintaining viral suppression through antiretroviral therapy can reduce the risk of transmission through breastfeeding to below 1%, but not zero. For HIV-infected individuals receiving antiretroviral therapy with a persistently low viral load, breastfeeding should be encouraged if they choose to do so. If viral load is not suppressed, pasteurized donor breast milk or formula is recommended.
For treating maternal hepatitis B, there is no difference in infection rates between breastfed and formula-fed infants, provided the infant receives hepatitis B immunoglobulin and hepatitis B vaccine at birth. Hepatitis B mothers are encouraged to breastfeed after their infants have received these prophylactic measures. When using tenofovir 200 mg and emtricitabine 300 mg for HIV pre-exposure prophylaxis, the infant receives only about 0.5% of the emtricitabine treatment dose. During prolonged daily administration of emtricitabine 200 mg by the mother, the drug concentration in the blood of breastfed infants is typically undetectable.
◉ Effects on breastfed infants
In one study, 50 infants breastfed by HIV-negative mothers received 10 days of pre-exposure prophylaxis, taking a combination of tenofovir disoproxil fumarate 300 mg and emtricitabine 200 mg daily, and were under direct observation. Two infants were reported to experience diarrhea lasting 2 to 3 days. No other side effects were reported.
◉ Effects on breastfeeding and breast milk
As of the revision date, no relevant published information was found.

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Protein binding Emtricitabine binds to <4% of plasma proteins, primarily serum albumin.

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1. Reproductive toxicity:
- In mice, emtricitabine (BW1592) (500 mg/kg/day, orally) resulted in a mild decrease in fetal weight (8% ± 2%), but no teratogenicity or embryonic resorption was observed [3]
- In rabbits, emtricitabine (100 mg/kg/day, orally) resulted in a decrease in fetal weight (10% ± 3%), but no malformations were observed [3]
2. Endothelial cell effects:
- In human umbilical vein endothelial cells (HUVECs), emtricitabine (BW1592) (20 μM) increased PARP activity by 2.1-fold and decreased NO production by 35% ± 4% (without cell death) [4]
3. Hepatic and renal safety:
- In rats, continuous 28 After oral administration of emtricitabine (BW1592) (300 mg/kg/day), no significant changes were observed in serum ALT, AST, creatinine, or BUN [1]. 4. Acute toxicity: The median lethal dose (LD50) of emtricitabine (BW1592) in mice was > 2000 mg/kg, and the median lethal dose (LD50) of emtricitabine (BW1592) in rats was > 1500 mg/kg [1].

[1]. Emtricitabine, a new antiretroviral agent with activity against HIV and hepatitis B virus. Clin Infect Dis.?2006 Jan 1;42(1):126-31.

[2]. Combined Medication of Antiretroviral Drugs Tenofovir Disoproxil Fumarate, Emtricitabine, and Raltegravir Reduces Neural Progenitor Cell Proliferation In Vivo and In Vitro. J Neuroimmune Pharmacol. 2017 Dec;12(4):682-692.

[3]. Szczech GM, Wang LH, Walsh JP, Reproductive toxicology profile of emtricitabine in mice and rabbits. Reprod Toxicol. 2003 Jan-Feb;17(1):95-108.

[4]. Effect of the Anti-retroviral Drugs Efavirenz, Tenofovir and Emtricitabine on Endothelial Cell Function: Role of PARP. Cardiovasc Toxicol. 2017 Jan 3. [Epub ahead of print].

Emtricitabine is an organofluorine compound with the structure 5-fluorocytosine substituted at position 1 with 2-(hydroxymethyl)-1,3-oxothiacyclopentane-5-yl (2R,5S configuration). It is used in combination therapy for HIV-1 infection. Emtricitabine has both antiviral and HIV-1 reverse transcriptase inhibitor effects. It is a pyrimidinone compound, organofluorine compound, monothioacetal, and nucleoside analog. Emtricitabine (brand name: emtricitabine) is a prescription drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of HIV infection in adults, children, and infants. Emtricitabine is always used in combination with other anti-HIV drugs. Emtricitabine is a nucleoside reverse transcriptase inhibitor (NRTI) indicated for the treatment of HIV infection in adults, or in combination with tenofovir alafenamide for the prevention of HIV-1 infection in high-risk adolescents and adults. Emtricitabine is a cytidine analog. This drug works by inhibiting HIV reverse transcriptase, preventing HIV RNA from being transcribed into DNA. Emtricitabine was approved by the U.S. Food and Drug Administration (FDA) on July 2, 2003. Racivir, also known as RCV, is an oxothiacyclopentane nucleoside reverse transcriptase inhibitor similar to emtricitabine and lamivudine. Racivir is a 50:50 mixture of emtricitabine and its enantiomers. Racivir has been used in clinical trials for the prevention of HIV infection. Emtricitabine is a human immunodeficiency virus nucleoside analog reverse transcriptase inhibitor. Its mechanism of action is as a nucleoside reverse transcriptase inhibitor. Emtricitabine is a nucleoside analog and reverse transcriptase inhibitor used in combination with other drugs for the treatment and prevention of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS). Emtricitabine does not appear to be a major cause of drug-induced liver injury, but it may exacerbate the condition of patients with co-infection with chronic hepatitis B virus (HBV). Emtricitabine is a synthetic fluorinated derivative of thiocytidine with potent antiviral activity. Emtricitabine is phosphorylated intracellularly to form emtricitabine 5'-triphosphate. This metabolite inhibits the activity of human immunodeficiency virus (HIV) reverse transcriptase by competing with the natural substrate deoxycytidine 5'-triphosphate and by incorporating into viral DNA, leading to DNA chain elongation termination (due to the lack of the essential 3'-OH group). Emtricitabine is a deoxycytidine analog and reverse transcriptase inhibitor with antiviral activity against HIV-1 and hepatitis B virus. It is used to treat HIV infection.

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Drug Indications
Emtricitabine is indicated for the treatment of HIV-1 infection in combination with other drugs; for the treatment of HIV-1 infection in children weighing 25-35 kg; for the treatment of HIV-1 infection in adults weighing ≥35 kg; for HIV-1 pre-exposure prophylaxis in adolescents and adults, excluding patients with a history of vaginal intercourse; for the treatment of HIV-1 infection in children and adults weighing ≥17 kg; for pre-exposure prophylaxis in adolescents and adults weighing ≥35 kg; for the treatment of HIV-1 infection in patients weighing ≥35 kg and aged ≥12 years; for the treatment of HIV-1 infection in patients weighing ≥35 kg; for the treatment of HIV-1 infection in patients weighing ≥25 kg; and for the treatment of HIV-1 infection in patients weighing ≥40 kg.
FDA Label
Emtricitabine (Emtriva) is indicated for the treatment of HIV-1 infection in adults and children in combination with other antiretroviral drugs. This indication is based on studies in treatment-naïve patients and previously treated patients with stable virological control. There is currently no experience with emtricitabine for treating patients who have failed current or multiple treatment regimens. When selecting a new treatment option for patients who have failed antiretroviral therapy, careful consideration should be given to drug-related mutation patterns and the patient's individual treatment history. Resistance testing may be appropriate when feasible.

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Mechanism of Action
Emtricitabine is a cytidine analog that, when phosphorylated to emtricitabine 5'-triphosphate, competes with deoxycytidine 5'-triphosphate for HIV-1 reverse transcriptase. Since HIV-1 reverse transcriptase incorporates emtricitabine into the forming DNA chain, new nucleotides cannot be incorporated, leading to viral DNA chain termination. Inhibiting reverse transcriptase prevents viral RNA from being transcribed into DNA, thus preventing the virus from incorporating its DNA into the host DNA and replicating using host cellular mechanisms. This reduces viral load.
Emtricitabine is a synthetic cytosine nucleoside analog that is phosphorylated by cellular enzymes to form emtricitabine 5'-triphosphate. Emtricitabine 5'-triphosphate inhibits HIV-1 reverse transcriptase activity by competing with the natural substrate deoxycytidine 5'-triphosphate and incorporating into neoviral DNA, leading to chain termination. Emtricitabine 5'-triphosphate is a weak inhibitor of mammalian DNA polymerases α, β, ε and mitochondrial DNA polymerase γ.

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1. Emtricitabine (BW1592) is a nucleoside reverse transcriptase inhibitor (NRTI) whose mechanism of action is to terminate viral DNA chain elongation by competitively binding to HIV RT/HBV DNA polymerase with natural deoxycytidine triphosphate (dCTP)[1]
2. Therapeutic indications include:
- HIV-1 treatment: often used in combination with tenofovir disoproxil fumarate (Truvada®) as a base drug for antiretroviral therapy[1][2]
- HIV pre-exposure prophylaxis (PrEP): used in combination with tenofovir disoproxil fumarate to reduce the risk of HIV infection in high-risk populations[1]
- Chronic hepatitis B treatment: reduces hepatitis B virus DNA levels and improves liver function[1]
3. In vitro studies have shown that emtricitabine, in combination with tenofovir disoproxil fumarate and raltelapir, can synergistically inhibit the proliferation of neural progenitor cells, therefore pregnant women should use it with caution[2]
4. Emtricitabine has low plasma protein binding and high oral bioavailability, making it suitable for once-daily oral administration [1].

C8H10FN3O3S

247.25

247.042

143491-57-0

Emtricitabine-13C,15N2;1217820-69-3;Emtricitabine-15N,d2;2714436-53-8

60877

White to off-white solid powder

1.8±0.1 g/cm3

443.3±55.0 °C at 760 mmHg

136-140°C

221.9±31.5 °C

0.0±2.4 mmHg at 25°C

1.731

-0.41

115.67

2

5

2

16

374

2

C1[C@H](O[C@H](S1)CO)N2C=C(C(=NC2=O)N)F

XQSPYNMVSIKCOC-NTSWFWBYSA-N

InChI=1S/C8H10FN3O3S/c9-4-1-12(8(14)11-7(4)10)5-3-16-6(2-13)15-5/h1,5-6,13H,2-3H2,(H2,10,11,14)/t5-,6+/m0/s1

4-amino-5-fluoro-1-[(2R,5S)-2-(hydroxymethyl)-1,3-oxathiolan-5-yl]pyrimidin-2-one

BW-1592; BW1592; BW 1592; trade names: Coviracil; Emtriva; Racivir; (-)-FTC; W-201247; W-201248; E1007; 24229-EP2298783A1; 24229-EP2314590A1; AB01275429-01; 3B2-0188

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 2.5 mg/mL (10.11 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (10.11 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (10.11 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。