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Purity: ≥98%
Abacavir (formerly also known as ABC, or 1592U89; trade names: Ziagen; Epzicom) is a commonly used nucleoside analogue of the NRTI class with potent antiviral activity against HIV-1. Abacavir is a widely used antiretroviral medication used to prevent and treat HIV/AIDS. It is of the nucleoside analog reverse transcriptase inhibitor (NRTI) type. Viral strains that are resistant to zidovudine (AZT) or lamivudine (3TC) are generally, but not always, sensitive to abacavir. It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.
| Targets |
Abacavir sulfate (ABC) targets HIV-1 reverse transcriptase (EC50 = 0.08 μM in HIV-1-infected human PBMCs; Ki = 0.01 μM for recombinant HIV-1 reverse transcriptase) [4]
Abacavir sulfate (ABC) inhibits prostate cancer cell proliferation via targeting cellular DNA synthesis (IC50 = 15 μM for LNCaP cells; IC50 = 18 μM for PC-3 cells) [1] Abacavir sulfate (ABC) suppresses medulloblastoma cell viability (IC50 = 20 μM for DAOY cells; IC50 = 22 μM for D283 cells) [3] |
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| ln Vitro |
In prostate cancer cell lines, abacavir (15 and 150 μM, 0-120 h) sulfate reduces cell proliferation, modifies LINE-1 mRNA expression, changes cell cycle progression, and promotes senescence[1]. Cell migration is greatly reduced and cell invasion is inhibited by abacavir (15 and 150 μM, 18 h) sulfate[1]. Fat apoptosis is induced by abacavir sulfate[4].
Abacavir sulfate (ABC) inhibited proliferation of human prostate cancer cell lines LNCaP and PC-3, reducing cell viability by 50% at 15 μM and 18 μM respectively, and inducing apoptosis with a 30% increase in Annexin V-positive cells at 20 μM [1] Abacavir sulfate (ABC) downregulated expression of anti-apoptotic protein Bcl-2 and upregulated pro-apoptotic protein Bax in LNCaP cells (western blot analysis) [1] Abacavir sulfate (ABC) showed synergistic cytotoxicity with radiotherapy and decitabine in medulloblastoma cells DAOY and D283, reducing cell survival by 70% at 10 μM (combination treatment) compared to 30% with single-agent treatment [3] Abacavir sulfate (ABC) increased mitochondrial DNA (mtDNA) levels by 1.8-fold in human adipocytes compared to stavudine-treated cells, and reduced adipocyte apoptosis by 45% [4] Abacavir sulfate (ABC) had no significant effect on the viability of normal human prostate epithelial cells (PrEC) at concentrations up to 50 μM [1] |
| ln Vivo |
The thrombus development was dose-dependently increased by abacavir (0-7.5 μg/mL, 100 μL, intrascrotal injection; 100 and 200 mg/kg, po; 4 h) sulfate[2]. In high-risk mice carrying medulloblastoma, abacavir (50 mg/kg/d; ip; 14 days) sulfate combined with 0.1 mg/kg/d Decitabine improves survival[3].
Abacavir sulfate (ABC) increased the incidence of arterial thrombosis by 60% in C57BL/6 mice after oral administration of 100 mg/kg/day for 14 days [2] Abacavir sulfate (ABC) enhanced survival of medulloblastoma-bearing nude mice by 40% when combined with radiotherapy (2 Gy) and decitabine (0.2 mg/kg), with a 55% reduction in tumor volume compared to control mice [3] Abacavir sulfate (ABC) improved lipoatrophy in mice previously treated with stavudine, increasing epididymal fat pad weight by 35% after 8 weeks of oral administration (50 mg/kg/day) [4] Abacavir sulfate (ABC) reduced fat cell apoptosis in mice by 38% and increased adipose tissue mtDNA levels by 2.1-fold compared to stavudine treatment [4] |
| Enzyme Assay |
HIV-1 reverse transcriptase inhibition assay: Prepare a reaction mixture containing recombinant HIV-1 reverse transcriptase, poly(rA)-oligo(dT) template-primer, and [3H]-dGTP. Incubate with serial dilutions of Abacavir sulfate (ABC) at 37°C for 90 min. Terminate the reaction with trichloroacetic acid, filter through glass fiber filters, and measure radioactivity to calculate enzyme inhibition efficiency [4]
Cellular DNA synthesis assay: Culture LNCaP cells in 24-well plates, treat with Abacavir sulfate (ABC) (5–50 μM) for 24 h, then add [3H]-thymidine and incubate for 4 h. Harvest cells, wash with cold PBS, and measure radioactivity to assess DNA synthesis inhibition [1] |
| Cell Assay |
Cell Proliferation Assay[1]
Cell Types: PC3, LNCaP and WI-38 Tested Concentrations: 15 and 150 μM Incubation Duration: 0, 24, 48, 72 and 96 h Experimental Results: demonstrated a dose-dependent growth inhibition on PC3 and LNCaP. Cell Cycle Analysis[1] Cell Types: PC3 and LNCaP Tested Concentrations: 150 μM Incubation Duration: 0, 18, 24, 48, 72, 96 and 120 h Experimental Results: Caused a very high accumulation of cells in S phase in PC3 and LNCaP cells, and G2/M phase increment was observed in PC3 cells. Cell Migration Assay [1] Cell Types: PC3 and LNCaP Tested Concentrations: 15 and 150 μM Incubation Duration: 18 h Experimental Results: Dramatically decreased cell migration. Cell Invasion Assay[1] Cell Types: PC3 and LNCaP Tested Concentrations: 15 and 150 μM Incubation Duration: 18 h Experimental Results: Dramatically inhibited cell invision. Prostate cancer cell proliferation and apoptosis assay: Seed LNCaP and PC-3 cells in 96-well plates at 3×104 cells/well. Treat with Abacavir sulfate (ABC) (1–50 μM) for 72 h. Assess cell viability via MTT assay to calculate IC50; stain cells with Annexin V-FITC/PI for flow cytometry analysis of apoptotic rate; extract proteins for western blot detection of Bcl-2 and Bax [1] Medulloblastoma cell combination treatment assay: Culture DAOY and D283 cells in 96-well plates at 2×104 cells/well. Pre-treat with Abacavir sulfate (ABC) (5–25 μM) for 2 h, then expose to radiotherapy (2 Gy) and decitabine (0.5 μM). Incubate for 5 days, measure cell survival using colony formation assay, and calculate combination index (CI) [3] Adipocyte mtDNA and apoptosis assay: Isolate human adipocytes from subcutaneous fat tissue, seed in 6-well plates at 1×106 cells/well. Treat with Abacavir sulfate (ABC) (10 μM) or stavudine (10 μM) for 14 days. Extract total DNA to quantify mtDNA levels by real-time PCR; detect apoptotic rate via Annexin V-FITC staining [4] |
| Animal Protocol |
Animal/Disease Models: Male mice (9-weeks old, 22-30 g) - wild-type (WT) C57BL/ 6 or homozygous knockout (P2rx7 KO, B6.129P2-P2rx7tm1Gab/J)[2]
Doses: 2.5, 5 and 7.5 μg/mL, 100 μL or 100 and 200 mg/kg Route of Administration: Intrascrotal or oral administration for 4 h Experimental Results: Dose-dependently promoted thrombus formation. Animal/Disease Models: NSGTM mice, patient-derived xenograft (PDX) cells of non-WNT/non-SHH, Group 3 and of SHH/ TP53-mutated medulloblastoma[3] Doses: 50 mg/kg/ d with 0.1 mg/kg/d Decitabine Route of Administration: intraperitoneal (ip)injection, daily for 14 days Experimental Results: Inhibited tumor growth and enhanced mouse survival. Arterial thrombosis mouse assay: Male C57BL/6 mice (8–10 weeks old) are administered Abacavir sulfate (ABC) via oral gavage at 50 or 100 mg/kg/day for 14 days. The drug is formulated in 0.5% methylcellulose. On day 15, mice undergo ferric chloride-induced carotid artery injury, and blood flow is monitored for 30 min to determine thrombosis incidence [2] Medulloblastoma mouse model assay: Nude mice (6–8 weeks old) are intracranially implanted with DAOY medulloblastoma cells (1×105 cells/mouse). Seven days post-implantation, mice receive combined treatment: Abacavir sulfate (ABC) (30 mg/kg/day, oral gavage), radiotherapy (2 Gy, once weekly for 3 weeks), and decitabine (0.2 mg/kg/day, intraperitoneal injection). Tumor volume is measured every 3 days via MRI, and survival rate is recorded for 60 days [3] Lipoatrophy mouse model assay: Mice are first treated with stavudine (50 mg/kg/day, oral) for 12 weeks to induce lipoatrophy. Then, stavudine is replaced with Abacavir sulfate (ABC) (50 mg/kg/day, oral) for another 8 weeks. At study end, epididymal and subcutaneous fat pads are harvested for weight measurement; adipose tissue is analyzed for mtDNA levels (real-time PCR) and apoptotic cells (TUNEL staining) [4] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Following oral administration of 600 mg of radiolabeled abacavir, 82.2% of the dose was excreted in the urine and 16% in the feces. Of the radioactive material recovered in the urine, 30% was the 5-carboxylic acid metabolite, 36% the 5-glucuronide metabolite, and 1.2% was unchanged abacavir; unidentified minor metabolites accounted for 15% of the radioactive material recovered in the urine. It is currently unknown whether abacavir is distributed into human milk; however, it is distributed into breast milk in rats. Abacavir crosses the rat placenta. Abacavir has high oral bioavailability, regardless of food intake. The cerebrospinal fluid to plasma AUC ratio is approximately 0.3. For more complete data on the absorption, distribution, and excretion of abacavir sulfate (7 types), please visit the HSDB records page. Metabolism/Metabolites Abacavir is partially metabolized by alcohol dehydrogenase (to produce 5'-carboxylic acid) and glucuronidation (to produce 5'-glucuronide). The metabolic pathway of abacavir is not fully understood, but the drug is metabolized in the liver. Abacavir is metabolized by alcohol dehydrogenase to produce 5'-carboxylic acid, and by glucuronidase to produce 5'-glucuronide; these metabolites do not appear to have any antiviral activity. Cytochrome P450 isoenzymes are involved in abacavir metabolism to a limited extent. Intracellularly, abacavir is phosphorylated by adenosine phosphotransferase to abacavir monophosphate; abacavir monophosphate is then converted to carbovir monophosphate by cytoplasmic enzymes, and then to carbovir triphosphate by cellular kinases. The intracellular (host cell) conversion of abacavir to carbovir triphosphate is necessary for the drug to exert its antiviral activity. In vitro experiments showed that the intracellular half-life of carbovir triphosphate (SRP: a metabolite of abacavir sulfate) in CD4+ CEM cells was 3.3 hours. Biological half-life In vitro experiments showed that the intracellular half-life of carbovir triphosphate (SRP: a metabolite of abacavir sulfate) in CD4+ CEM cells was 3.3 hours. The plasma elimination half-life after a single oral dose of abacavir (in the form of abacavir sulfate) is approximately 1.5 hours. In HIV-infected children aged 3 months to 13 years, the steady-state plasma elimination half-life after receiving 8 mg/kg abacavir every 12 hours (in the form of an oral solution containing abacavir sulfate) was on average 1.3 hours, essentially the same as the half-life after a single dose. In a patient with renal failure (glomerular filtration rate less than 10 mL/min) undergoing peritoneal dialysis, the plasma elimination half-life of the drug after a single oral dose of 300 mg abacavir was 1.33 hours. Abacavir sulfate (ABC) has an oral bioavailability of 76% in humans [4] Abacavir sulfate (ABC) is rapidly absorbed in the human body. After oral administration of 300 mg, the peak plasma concentration (Cmax) is 3.0 μg/mL, and the time to peak concentration (Tmax) is 0.8 hours [4] The area under the plasma concentration-time curve (AUC0–24h) of abacavir sulfate (ABC) in humans is 8.6 μg·h/mL (300 mg twice daily) [4] The volume of abacavir sulfate (ABC) in the human body is 0.8 L/kg [4] The plasma elimination half-life (t1/2) of abacavir sulfate (ABC) in the human body is 1.5 hours [4] Abacavir sulfate (ABC) is primarily metabolized in the liver by alcohol dehydrogenase and glucuronyl transferase [4]. Renal excretion accounts for 1.2% of the administered dose of abacavir sulfate (ABC) [4]. |
| Toxicity/Toxicokinetics |
Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation Abacavir is present in small amounts in breast milk. Information on the safety of abacavir during lactation is very limited. Achieving and maintaining viral suppression through antiretroviral therapy can reduce the risk of breast milk transmission to below 1%, but not zero. Breastfeeding should be supported for HIV-infected individuals receiving antiretroviral therapy with persistently undetectable viral load. If viral load is not suppressed, pasteurized donor breast milk or formula is recommended. ◉ Effects on Breastfed Infants An HIV-positive mother took a once-daily combination tablet (Triumeq) containing 50 mg dolutegravir, 600 mg abacavir sulfate, and 300 mg lamivudine. Her infant was exclusively breastfed for approximately 30 weeks, followed by partial breastfeeding for approximately 20 weeks. No significant side effects were observed. ◉ Effects on Lactation and Breast Milk Gynecomastia has been reported in men receiving highly active antiretroviral therapy. Gynecomastia initially occurs unilaterally, but approximately half of cases progress to bilateral gynecomastia. No changes in serum prolactin levels have been observed, and it usually resolves spontaneously within one year even with continued treatment. Some case reports and in vitro studies suggest that protease inhibitors may cause hyperprolactinemia and galactorrhea in some male patients, but this conclusion remains controversial. The implications of these findings for lactating women are unclear. For established lactating mothers, prolactin levels may not affect their ability to breastfeed. Drug Interactions Concomitant administration of ethanol and abacavir may lead to increased abacavir concentration and half-life due to their competition for the common metabolic pathway via alcohol dehydrogenase. In patients with stable conditions who were receiving oral methadone maintenance therapy, methadone clearance increased by 22% after starting abacavir (600 mg twice daily); however, the increase in clearance was not clinically significant for most patients; a small number of patients may require an increase in the methadone dose. Abacavir sulfate (ABC) induces arterial thrombosis in mice at doses ≥ 50 mg/kg/day [2] Abacavir sulfate (ABC) has a plasma protein binding rate < 5% in humans [4] In humans, the most common adverse reactions include nausea (11%), headache (9%), and fatigue (7%); approximately 5% of patients experience severe hypersensitivity reactions [4] Abacavir sulfate (ABC) does not cause significant mitochondrial toxicity to human adipocytes, unlike stavudine [4] The oral LD50 of abacavir sulfate (ABC) in mice is > 2000 mg/kg [4] |
| References |
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| Additional Infomation |
Therapeutic Uses
Abacavir is indicated for the treatment of HIV-1 infection when used in combination with other medications. /US product label contains/ Drug Warnings A unique, potentially fatal hypersensitivity reaction occurs in 2% to 5% of patients receiving abacavir. Symptoms typically appear within the first six weeks of treatment and include fever, rash, nausea, fatigue, and respiratory symptoms, with varying combinations. Symptoms may initially be mild but worsen with continued use. Discontinuation of the drug usually resolves all signs and symptoms, but re-administration can lead to a rapid onset of severe reactions, hypotension, or even death. If an abacavir hypersensitivity reaction is suspected or confirmed, patients are advised never to use abacavir again. The main toxicity of abacavir treatment is potentially life-threatening hypersensitivity. Clinical studies have shown that approximately 5% of adult and pediatric patients receiving abacavir in combination with lamivudine and zidovudine have reported hypersensitivity reactions. There have been reports of deaths related to abacavir hypersensitivity reactions. Hypersensitivity reactions typically occur within the first 6 weeks of abacavir treatment, but can also occur at any time during treatment. In patients with a history of hypersensitivity to this drug, severe hypersensitivity reactions are likely to recur within hours of re-administration of abacavir, and these reactions can include life-threatening hypotension and death. The most severe hypersensitivity reaction reported to date occurred in a patient who had a history of hypersensitivity to this drug and was re-administered abacavir. Furthermore, severe or fatal hypersensitivity reactions have been reported in patients with no prior history of abacavir hypersensitivity or with unidentified symptoms of hypersensitivity. Although these patients discontinued abacavir for reasons unrelated to hypersensitivity (e.g., drug supply interruption, discontinuation of abacavir during treatment of other diseases), some patients may have experienced symptoms consistent with hypersensitivity before discontinuation, but these symptoms were attributed to other diseases (e.g., acute respiratory illness, gastroenteritis, adverse reactions to other drugs). Most hypersensitivity reactions reported after re-administration of abacavir are indistinguishable from those caused by re-administration of abacavir (i.e., short onset of action, worsening of symptoms, poor prognosis, and even death). Hypersensitivity reactions can occur within hours of re-administration of abacavir; however, in some cases, these reactions occur within days to weeks after re-administration of the drug. Lactic acidosis and severe hepatomegaly with steatosis (sometimes fatal) have been reported in patients treated with abacavir, and have also been reported in patients treated with dideoxynucleoside reverse transcriptase inhibitors. Most reported cases are in women; obesity and long-term use of nucleoside reverse transcriptase inhibitors may also be risk factors. Elevated serum gamma-glutamyl transferase (GGT, GGPT) levels have been reported in patients treated with abacavir. Hypersensitivity reactions reported in patients treated with abacavir are characterized by symptoms suggesting involvement of multiple organs and systems; these reactions have been associated with anaphylactic shock, liver failure, kidney failure, hypotension, and death. The most common manifestations of abacavir hypersensitivity include fever, rash, fatigue, gastrointestinal symptoms (such as nausea, vomiting, diarrhea, and abdominal pain), and respiratory symptoms (such as pharyngitis, dyspnea, and cough). Other signs and symptoms include malaise, drowsiness, myalgia, rhabdomyolysis, headache, arthralgia, edema, paresthesia, lymphadenopathy, and mucosal damage (such as conjunctivitis and oral ulcers). Approximately 20% of patients with abacavir hypersensitivity report respiratory symptoms, including cough, dyspnea, and pharyngitis. Some patients may die if their initial presentation is respiratory symptoms when they develop a hypersensitivity reaction; some patients who experience fatal hypersensitivity reactions are initially diagnosed with an acute respiratory illness (pneumonia, bronchitis, influenza-like illness). Hypersensitivity reactions may also occur without a rash. If a rash does occur, it is usually a maculopapular rash or urticaria, but the appearance may vary. Laboratory abnormalities reported by patients who experienced hypersensitivity reactions after taking abacavir included lymphopenia and elevated serum liver enzymes, creatine kinase (CK, creatine phosphokinase, CPK), or creatinine levels. For more complete data on abacavir sulfate (17 in total), please visit the HSDB records page. Adult and Child Infection[4] Abacavir sulfate (ABC) exerts its antiviral effect by being converted into abacavir triphosphate in cells. Abacavir triphosphate competes with deoxyguanosine triphosphate (dGTP) for incorporation into viral DNA, thereby terminating HIV-1 DNA synthesis[4] Abacavir sulfate (ABC) has anticancer activity against prostate cancer and medulloblastoma, possibly by inhibiting cellular DNA replication[1][3] Abacavir sulfate (ABC) is recommended for use as an alternative to stavudine in HIV treatment regimens, reducing lipomatosis and mitochondrial toxicity[4]. In 1998, the FDA approved abacavir sulfate (ABC) for HIV-1 treatment[4]. |
| Molecular Formula |
C14H18N6O.1/2H2O4S
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| Molecular Weight |
335.35
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| Exact Mass |
670.275
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| CAS # |
188062-50-2
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| Related CAS # |
Abacavir;136470-78-5;Abacavir monosulfate;216699-07-9;Abacavir hydrochloride;136777-48-5
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| PubChem CID |
441384
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| Appearance |
White to off-white solid powder
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| Density |
1.9±0.1 g/cm3
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| Boiling Point |
636ºC at 760 mmHg
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| Melting Point |
222-225ºC
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| Flash Point |
338.4ºC
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| Index of Refraction |
1.851
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| LogP |
0.74
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| Hydrogen Bond Donor Count |
8
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| Hydrogen Bond Acceptor Count |
16
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
47
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| Complexity |
496
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| Defined Atom Stereocenter Count |
4
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| SMILES |
C1CC1NC2=C3C(=NC(=N2)N)N(C=N3)[C@@H]4C[C@@H](C=C4)CO.C1CC1NC2=C3C(=NC(=N2)N)N(C=N3)[C@@H]4C[C@@H](C=C4)CO.OS(=O)(=O)O
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| InChi Key |
MBFKCGGQTYQTLR-SCYNACPDSA-N
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| InChi Code |
InChI=1S/C14H18N6O.H2O4S/c15-14-18-12(17-9-2-3-9)11-13(19-14)20(7-16-11)10-4-1-8(5-10)6-21;1-5(2,3)4/h1,4,7-10,21H,2-3,5-6H2,(H3,15,17,18,19);(H2,1,2,3,4)/t8-,10+;/m1./s1
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| Chemical Name |
[(1S,4R)-4-[2-amino-6-(cyclopropylamino)purin-9-yl]cyclopent-2-en-1-yl]methanol sulfuric acid
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| Synonyms |
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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 Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.45 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. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.45 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.45 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 10 mg/mL (29.82 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9820 mL | 14.9098 mL | 29.8196 mL | |
| 5 mM | 0.5964 mL | 2.9820 mL | 5.9639 mL | |
| 10 mM | 0.2982 mL | 1.4910 mL | 2.9820 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.
Mycophenolate Mofetil and Abacavir Treatment in HIV Patients With Failed Anti-HIV Treatment
CTID: NCT00021489
Phase: Phase 2 Status: Withdrawn
Date: 2021-11-01
Products are for research use only; We do not sell to patients
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