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]

Emtricitabine exhibits in vitro efficacy against clinical isolates of HIV-1 as well as laboratory strains of HIV-1 and HIV-2. EC50, or the 50% effective concentration, varies between 0.002 to 1.5 μmol/L based on the cell line and virus isolate employed. When paired with didanosine or zalcitabine, emtricitabine is active in vitro and synergizes with stavudine and zidovudine in vitro [1].

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1. Antiviral activity against HIV and HBV:
- In HIV-1-infected human PBMCs, Emtricitabine (BW1592) (0.01–0.1 μM) dose-dependently reduced HIV-1 p24 antigen: 0.05 μM reduced p24 by 90% ± 4%; 0.1 μM achieved >95% inhibition [1]
- In HepG2.2.15 cells, Emtricitabine (0.05–0.5 μM) decreased HBV DNA levels by 50% ± 3% (0.1 μM) and 80% ± 4% (0.5 μM) (real-time PCR) [1]
2. Inhibition of neural progenitor cell (NPC) proliferation:
- In mouse embryonic NPCs (neurosphere culture), Emtricitabine (BW1592) (10 μM) alone reduced neurosphere formation rate by 22% ± 3%; combined with Tenofovir DF (10 μM) and Raltegravir (1 μM), the rate decreased by 55% ± 5% (Nestin immunostaining) [2]
- NPC proliferation (EdU incorporation) was reduced by 18% ± 2% (10 μM alone) and 48% ± 4% (triple combination) [2]
3. Impairment of endothelial cell function:
- In human umbilical vein endothelial cells (HUVECs), Emtricitabine (BW1592) (5–20 μM) dose-dependently increased PARP activity (2.1-fold at 20 μM) and decreased nitric oxide (NO) production (↓35% ± 4% at 20 μM) [4]
- At 20 μM, Emtricitabine did not affect HUVEC viability (MTT assay, viability >90% vs. control) [4]

Emtricitabine was used in toxicity research related to reproduction and development. The daily area under the curve (AUC0→24) for exposure to pregnant animals at oral dosages up to 1000 mg/kg/day once daily is around 60- to 120-fold (mouse to rabbit), greater than the recommended amount for humans ( 200 mg). Emtricitabine had no effect on sperm count, early embryonic development, or fertility in a mouse fertility research. Studies on the embryofetal toxicity of mice and rabbits did not reveal a higher prevalence of abnormalities. Emtricitabine had no effect on the development or fertility of F1 offspring in prenatal or postnatal trials conducted in mice. According to these findings, emtricitabine has a favorable preclinical safety profile for reproduction [2].

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1. Antiviral efficacy in animal models:
- In HIV-1-infected SCID mice (human PBMC reconstituted), oral Emtricitabine (BW1592) (20 mg/kg/day) for 14 days reduced plasma HIV-1 RNA by 2.3 log10 copies/mL vs. control [1]
- In HBV-transgenic mice, oral Emtricitabine (30 mg/kg/day) for 21 days decreased hepatic HBV DNA by 65% ± 5% (Southern blot) [1]
2. Effect on fetal neural progenitor cells:
- Pregnant C57BL/6 mice treated with Emtricitabine (BW1592) (30 mg/kg/day, oral) from gestational day 10 to postnatal day 7:
- Postnatal offspring brain NPC proliferation (Ki67 staining) decreased by 20% ± 3% (vs. control) [2]
- No significant fetal mortality or neurohistological damage [2]
3. Reproductive toxicity in rodents:
- In CD-1 mice (oral Emtricitabine (BW1592) 50, 150, 500 mg/kg/day, gestational day 6–15):
- No increase in embryo resorption rate; fetal body weight decreased by 8% ± 2% at 500 mg/kg [3]
- In New Zealand White rabbits (oral 10, 30, 100 mg/kg/day, gestational day 6–18):
- No teratogenicity; fetal body weight decreased by 10% ± 3% at 100 mg/kg [3]

Reagent preparation: Recombinant HIV-1 RT was resuspended in assay buffer (50 mM Tris-HCl, pH 7.8, 7.5 mM MgCl₂, 50 mM KCl). Emtricitabine (BW1592) was dissolved in DMSO to serial concentrations (0.001–1 μM). Biotin-labeled poly(rC)-oligo(dG) (substrate) and digoxigenin-labeled dGTP were diluted in assay buffer [1]
- Experimental procedure: The 50 μL reaction system contained HIV-1 RT (0.4 μg), substrate (80 ng), dGTP (8 μM), and Emtricitabine (different concentrations). Incubation at 37°C for 45 minutes; reaction terminated with 20 μL 0.6 M EDTA [1]
- Detection and analysis: Mixture transferred to streptavidin-coated 96-well plates; after washing, anti-digoxigenin-HRP conjugate was added. TMB substrate was used for color development, and absorbance at 450 nm was measured. EC50 was calculated by fitting the dose-response curve [1]

1. Neural progenitor cell (NPC) assay :
- Cell isolation and culture: NPCs were isolated from E14.5 mouse embryonic forebrains and cultured in neurosphere medium (DMEM/F12 + 20 ng/mL EGF + 20 ng/mL bFGF + 2% B27) at 37°C with 5% CO₂ [2]
- Drug treatment: NPCs (1×10⁴ cells/well) were seeded in 96-well plates and treated with Emtricitabine (BW1592) (1, 5, 10 μM) alone or with Tenofovir DF (10 μM) + Raltegravir (1 μM) for 72 hours [2]
- Detection:
- Neurosphere formation: Counted under inverted microscope; formation rate = (experimental spheres/control spheres) × 100% [2]
- Proliferation: EdU incorporation assay (fluorescent staining, flow cytometry quantification) [2]
2. HUVEC endothelial cell assay :
- Cell culture: HUVECs were cultured in EGM-2 medium supplemented with 10% FBS at 37°C with 5% CO₂ [4]
- Drug treatment: Confluent HUVECs were treated with Emtricitabine (BW1592) (5, 10, 20 μM) for 24 hours; untreated cells served as control [4]
- Detection:
- PARP activity: Measured by colorimetric assay kit (absorbance at 405 nm) [4]
- NO production: Detected by Griess reagent (absorbance at 540 nm) [4]
- Cell viability: MTT assay (absorbance at 570 nm) [4]
3. HIV-1-infected PBMC assay :
- Cell preparation: Human PBMCs were isolated by Ficoll-Hypaque gradient centrifugation and activated with 5 μg/mL PHA + 10 U/mL IL-2 for 3 days [1]
- Infection and treatment: Activated PBMCs (1×10⁶ cells/mL) were infected with HIV-1IIIB (MOI=0.01) for 2 hours, then treated with Emtricitabine (0.005–0.1 μM) [1]
- Viral detection: HIV-1 p24 antigen in supernatant was measured by ELISA; viral RNA was quantified by real-time RT-PCR [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

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (10.11 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (10.11 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (10.11 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)