在前列腺癌细胞系中，阿巴卡韦（15 和 150 μM，0-120 小时）可减缓细胞生长、修改 LINE-1 mRNA 表达、促进衰老并改变细胞周期进程 [1]。阿巴卡韦（15 和 150 μM，18 小时）可大大减少细胞迁移并抑制细胞侵袭[1]。阿巴卡韦诱导脂肪细胞凋亡[4]。

剂量依赖性地，阿巴卡韦（100 和 200 mg/kg，口服；4 小时）会增加血栓形成 [2]。在患有高危髓母细胞瘤的小鼠中，阿巴卡韦（50 mg/kg/d；腹腔注射；14天）和地西他滨（0.1 mg/kg/d）可以提高存活率[3]。

细胞增殖测定 [1]
细胞类型： PC3、LNCaP 和 WI-38
测试浓度： 15 和 150 μM
孵育持续时间：0、24、48、72 和 96 小时
实验结果：PC3 和 LNCaP 具有剂量依赖性生长抑制作用。

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细胞周期分析 [1]
细胞类型： PC3 和 LNCaP
测试浓度： 150 μM
孵育持续时间：0、18、24、48、72、96和120小时
实验结果：引起PC3和LNCaP细胞以及An中S期细胞的大量积累在 PC3 细胞中观察到 G2/M 期增加。

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细胞迁移测定[1]
细胞类型： PC3 和 LNCaP
测试浓度： 15 和 150 μM
孵化持续时间：18小时
实验结果：细胞迁移显着减少。

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细胞侵袭测定[1]
细胞类型： PC3 和 LNCaP
测试浓度： 15 和 150 μM
孵育时间：18小时
实验结果：显着抑制细胞侵袭。

Animal/Disease Models: Male mouse (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 over 4 hrs (hrs (hours))
Experimental Results: Dose-dependent promotion of thrombosis.

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Animal/Disease Models: NSGTM mice, patient-derived xenograft (PDX) cells of non-WNT/non-SHH, group 3 and SHH/TP53 mutant medulloblastoma [3]
Doses: 50 mg/kg/d, 0.1 mg/kg /d Decitabine
Route of Administration: intraperitoneal (ip) injection, one time/day for 14 days
Experimental Results: Inhibited tumor growth and improved mouse survival.

Absorption, Distribution and Excretion
Rapid and extensive after oral administration (83% bioavailability, tablet). When a 300 mg tablet is given twice daily to subjects, the peak plasma concentration (Cmax) was 3.0 ± 0.89 mcg/mL and the area under the curve (AUC 0-12 hours) was 6.02 ± 1.73 mcg•hr/mL.
Elimination of abacavir was quantified in a mass balance study following administration of a 600-mg dose of 14C-abacavir: 99% of the radioactivity was recovered, 1.2% was excreted in the urine as abacavir, 30% as the 5′-carboxylic acid metabolite, 36% as the 5′-glucuronide metabolite, and 15% as unidentified minor metabolites in the urine. Fecal elimination accounted for 16% of the dose. Renal excretion of unchanged abacavir is a minor route of elimination in humans.
0.86 ± 0.15 L/kg [IV administration]
0.80 ± 0.24 L/hr/kg [asymptomatic, HIV-1-infected adult patients receiving single (IV dose of 150 mg]

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Metabolism / Metabolites
Hepatic, by alcohol dehydrogenase and glucuronosyltransferase to a 5′-carboxylic acid metabolite and 5′-glucuronide metabolite, respectively. These metabolites have no antiviral activity. Abacavir is not significantly metabolized by cytochrome P450 enzymes.

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Biological Half-Life
1.54 ± 0.63 hours

Hepatotoxicity
Elevations in serum aminotransferase levels above 5 times the upper limit of normal occur in up to 6% of patients on abacavir. These elevations are usually mild, transient and do not require dose adjustment. Clinically apparent hepatotoxicity is rare, but isolated cases [usually anicteric] have been published. The liver injury usually arises in the context of abacavir hypersensitivity syndrome and may be overshadowed by the allergic syndromes of fever, rash and fatigue. The onset is usually within 1 to 3 months of starting abacavir. The serum enzyme pattern can be hepatocellular or cholestatic. Patients typically recover rapidly within 4 weeks of stopping therapy.
Likelihood score: C (probable cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Abacavir appears in breastmilk in small quantities. Very little information is available on the safety of its use during breastfeeding. Achieving and maintaining viral suppression with antiretroviral therapy decreases breastfeeding transmission risk to less than 1%, but not zero. Individuals with HIV who are on antiretroviral therapy with a sustained undetectable viral load and who choose to breastfeed should be supported in this decision. If a viral load is not suppressed, banked pasteurized donor milk or formula is recommended.
◉ Effects in Breastfed Infants
An HIV-positive mother took a combination tablet containing dolutegravir 50 mg, abacavir sulfate 600 mg and lamivudine 300 mg (Triumeq) once daily. Her infant was exclusively breastfed for about 30 weeks and partially breastfed for about 20 weeks more. No obvious side effects were noted.
◉ Effects on Lactation and Breastmilk
Gynecomastia has been reported among men receiving highly active antiretroviral therapy. Gynecomastia is unilateral initially, but progresses to bilateral in about half of cases. No alterations in serum prolactin were noted and spontaneous resolution usually occurred within one year, even with continuation of the regimen. Some case reports and in vitro studies have suggested that protease inhibitors might cause hyperprolactinemia and galactorrhea in some male patients, although this has been disputed. The relevance of these findings to nursing mothers is not known. The prolactin level in a mother with established lactation may not affect her ability to breastfeed.

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Protein Binding
Moderate (approximately 50%). Binding of abacavir to plasma protein was independent of concentration.

[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.

Abacavir is a 2,6-diaminopurine that is (1S)-cyclopent-2-en-1-ylmethanol in which the pro-R hydrogen at the 4-position is substituted by a 2-amino-6-(cyclopropylamino)-9H-purin-9-yl group. A nucleoside analogue reverse transcriptase inhibitor (NRTI) with antiretroviral activity against HIV, it is used (particularly as the sulfate) with other antiretrovirals in combination therapy of HIV infection. It has a role as a HIV-1 reverse transcriptase inhibitor, an antiviral drug and a drug allergen.
Abacavir (brand name: Ziagen) is a prescription medicine approved by the U.S. Food and Drug Administration (FDA) for the treatment of HIV infection in adults, children, and infants. Abacavir is always used in combination with other HIV medicines. 
Abacavir (ABC) is a powerful nucleoside analog reverse transcriptase inhibitor (NRTI) used to treat HIV and AIDS. Chemically, it is a synthetic carbocyclic nucleoside and is the enantiomer with 1S, 4R absolute configuration on the cyclopentene ring. In vivo, abacavir sulfate dissociates to its free base, abacavir.
Abacavir is a Human Immunodeficiency Virus Nucleoside Analog Reverse Transcriptase Inhibitor. The mechanism of action of abacavir is as a Nucleoside Reverse Transcriptase Inhibitor, and Cytochrome P450 1A1 Inhibitor.
Abacavir sulfate is a nucleoside analogue and reverse transcriptase inhibitor which is used in combination with other agents in the therapy of the human immunodeficiency virus (HIV) infection and the acquired immunodeficiency syndrome (AIDS). Abacavir is a rare cause of clinically apparent drug induced liver injury.
Abacavir is a nucleoside reverse transcriptase inhibitor analog of guanosine. This agent decreases HIV viral loads, retards or prevents the damage to the immune system, and reduces the risk of developing AIDS.

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Drug Indication
Abacavir is indicated in combination with other anti-retroviral agents for the treatment of HIV-1 infection. It is available in a combination product alongside [dolutegravir] and [lamivudine] for the treatment of adult and pediatric patients with HIV-1 who weigh ≥10 kg.
FDA Label
Ziagen is indicated in antiretroviral combination therapy for the treatment of Human Immunodeficiency Virus (HIV) infection in adults, adolescents and children. The demonstration of the benefit of Ziagen is mainly based on results of studies performed with a twice daily regimen, in treatment-naïve adult patients on combination therapy. Before initiating treatment with abacavir, screening for carriage of the HLA-B*5701 allele should be performed in any HIV-infected patient, irrespective of racial origin. Abacavir should not be used in patients known to carry the HLA-B*5701 allele.

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Mechanism of Action
Abacavir is a carbocyclic synthetic nucleoside analogue and an antiviral agent. Intracellularly, abacavir is converted by cellular enzymes to the active metabolite carbovir triphosphate, an analogue of deoxyguanosine-5'-triphosphate (dGTP). Carbovir triphosphate inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA. Viral DNA growth is terminated because the incorporated nucleotide lacks a 3'-OH group, which is needed to form the 5′ to 3′ phosphodiester linkage essential for DNA chain elongation.

C14H18N6O

286.34

286.154

136470-78-5

Abacavir sulfate;188062-50-2;Abacavir monosulfate;216699-07-9;Abacavir hydrochloride;136777-48-5;Abacavir-d4;1260619-56-4;rel-Abacavir-d4;1217731-56-0

441300

White to off-white solid powder

1.7±0.1 g/cm3

636.0±65.0 °C at 760 mmHg

161 °C(dec.)

338.4±34.3 °C

0.0±2.0 mmHg at 25°C

1.864

0.72

101.88

3

6

4

21

414

2

C1CC1NC2=C3C(=NC(=N2)N)N(C=N3)[C@@H]4C[C@@H](C=C4)CO

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

EpzicomABC, Ziagen

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)

DMSO : ~100 mg/mL (~349.25 mM)
H2O : ~2 mg/mL (~6.98 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (8.73 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 (8.73 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 (8.73 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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配方 4 中的溶解度: 3.33 mg/mL (11.63 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 通过加热和超声助溶。

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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。