在前列腺癌细胞系中，阿巴卡韦盐酸盐（15 和 150 μM，0-120 小时）抑制细胞生长，修饰 LINE-1 mRNA 的表达，影响细胞周期的发育，并促进衰老[1]。盐酸阿巴卡韦（15 和 150 μM，18 小时）极大地抑制细胞迁移和侵袭[1]。盐酸阿巴卡韦可诱导脂肪细胞凋亡[4]。

盐酸阿巴卡韦在 100 和 200 mg/kg（口服）时剂量依赖性地促进血栓形成； 4 小时[2]。 0.1 mg/kg/d 地西他滨和 50 mg/kg/d 盐酸阿巴卡韦的组合（腹腔注射；14 天）可改善携带髓母细胞瘤的高危小鼠的存活率[3]。

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: Route 1: 2.5, 5, and 7.5 μg/mL, 100 μL Route 2: 100 and 200 mg/kg
Route of Administration: Intrascrotal or oral administration for 4 h
Experimental Results: Dose-dependently promoted thrombus formation.

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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.

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 from the 5-carboxylic acid metabolite, 36% from the 5-glucuronide metabolite, and 1.2% from the unchanged abacavir; unidentified minor metabolites accounted for 15% of the radioactive material recovered in the urine. It is unclear 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 metabolites), please visit the HSDB record page.

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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 (administered as abacavir sulfate) was 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 (administered as an oral solution containing abacavir sulfate) was on average 1.3 hours, essentially the same as the half-life after a single dose. In patients 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.

Effects During Pregnancy and Lactation
◉ Overview of Lactation Use
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. For HIV-infected individuals receiving antiretroviral therapy with a persistently low viral load, breastfeeding should be encouraged if chosen. 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 about half of the 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 mothers who have established lactation, prolactin levels may not affect their ability to breastfeed.

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Drug Interactions
Concomitant administration of ethanol and abacavir may lead to an increase in 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); for most patients, the increase in clearance was not clinically significant; a small number of patients may require an increase in the methadone dose.

[1]. The reverse transcription inhibitor abacavir shows anticancer activity in prostate cancer cell lines. PLoS One. 2010 Dec 3;5(12):e14221.

[2]. Abacavir Induces Arterial Thrombosis in a Murine Model. J Infect Dis. 2018 Jun 20;218(2):228-233.

[3]. Enhanced Survival of High-Risk Medulloblastoma-Bearing Mice after Multimodal Treatment with Radiotherapy, Decitabine, and Abacavir. Int J Mol Sci. 2022 Mar 30;23(7):3815.

[4]. Improvements in lipoatrophy, mitochondrial DNA levels and fat apoptosis after replacing stavudine with abacavir or zidovudine. AIDS. 2005 Jan 3;19(1):15-23.

Therapeutic Uses
Abacavir is indicated for the treatment of HIV-1 infection when used in combination with other medications. /US product label contains/

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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 have developed hypersensitivity to abacavir include lymphopenia and elevated serum liver enzymes, creatine kinase (CK, creatine phosphokinase, CPK), or creatinine levels. For more complete data on drug warnings for abacavir sulfate (17 in total), please visit the HSDB record page.

C28H38N12O6S

670.74312

670.276

136777-48-5

Abacavir;136470-78-5;Abacavir sulfate;188062-50-2;Abacavir monosulfate;216699-07-9

441384

White to off-white solid

3.921

286.74

8

16

8

47

496

4

S(=O)(=O)(O)O.OC[C@@H]1C=C[C@@H](C1)N1C=NC2C1=NC(N)=NC=2NC1CC1.OC[C@@H]1C=C[C@@H](C1)N1C=NC2C1=NC(N)=NC=2NC1CC1

MCGSCOLBFJQGHM-SCZZXKLOSA-N

InChI=1S/C14H18N6O/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/h1,4,7-10,21H,2-3,5-6H2,(H3,15,17,18,19)/t8-,10+/m1/s1

[(1S,4R)-4-[2-amino-6-(cyclopropylamino)purin-9-yl]cyclopent-2-en-1-yl]methanol

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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。