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3-脱氮腺苷盐酸盐
- names：
3-Deazaadenosine hydrochloride
- CAS号：
86583-19-9
MDL Number： - MF(分子式)： C11H15ClN4O4 MW(分子量)： 302.71
- EINECS: Reaxys Number:
- Pubchem ID:134828261 Brand:BIOFOUNT
3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)是一种S-腺苷高半胱氨酸水解酶（S-adenosylhomocysteine hydrolase）抑制剂，Ki 约为3.9 µM； 3-脱氮杂腺苷盐酸盐（盐酸盐）具有抗炎，抗增殖，抗HIV等活性。
| 货品编码 | 规格 | 纯度 | 价格 (¥) | 现价(¥) | 特价(¥) | 库存描述 | 数量 | 总计 (¥) |
|---|---|---|---|---|---|---|---|---|
| YZM000636-100mg | 100mg | 98.06% | ¥ 16000.00 | ¥ 16000.00 | 1-3天 | ¥ 0.00 | ||
| YZM000636-20mg | 20mg | 98.06% | ¥ 8600.00 | ¥ 8600.00 | 1-3天 | ¥ 0.00 | ||
| YZM000636-5mg | 5mg | 98.06% | ¥ 3948.00 | ¥ 3948.00 | 1-3天 | ¥ 0.00 | ||
| YZM000636-1mg | 1mg | 98.06% | ¥ 1755.00 | ¥ 1755.00 | 1-3天 | ¥ 0.00 |
| 中文别名 | 3-脱氮腺苷盐酸盐(86583-19-9);3-脱氮腺苷;盐酸3-脱氮腺苷;盐酸3-脱氮腺苷;3-去氮杂腺苷（盐酸盐);HY-W013332A;CS-0069568; |
| 英文别名 | 3-Deazaadenosine hydrochloride(86583-19-9);3-deazaadenosine;3-deazaadenosine hydrochloride;3-deazaadenosine hydrochloride;3-Deazaadenosine (hydrochloride):HY-W013332A;CS-0069568; |
| CAS号 | 86583-19-9 |
| SMILES | O[C@H]1[C@@H](O[C@H](CO)[C@H]1O)N2C3=C(C(N)=NC=C3)N=C2.Cl |
| Inchi | InChI=1S/C11H14N4O4.ClH/c12-10-7-5(1-2-13-10)15(4-14-7)11-9(18)8(17)6(3-16)19-11;/h1-2,4,6,8-9,11,16-18H,3H2,(H2,12,13);1H/t6-,8-,9-,11-;/m1./s1 |
| InchiKey | WQRKYGAAEYXMKZ-RPWKAPHTSA-N |
| 分子式 Formula | C11H15ClN4O4 |
| 分子量 Molecular Weight | 302.71 |
| 闪点 FP | No data available |
| 熔点 Melting point | No data available |
| 沸点 Boiling point | No data available |
| Polarizability极化度 | |
| 密度 Density | No data available |
| 蒸汽压 Vapor Pressure | |
| 溶解度Solubility | 生物体外In Vitro:DMSO溶解度41.67 mg/mL(137.66 mM;Need ultrasonic) |
| 性状 | Solid |
| 储藏条件 Storage conditions | 4°C, sealed storage, away from moisture * In solvent : -80°C, 6 months月; -20°C, 1 month月 (sealed storage, away from moisture) |
3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)实验注意事项：
1.实验前需戴好防护眼镜，穿戴防护服和口罩，佩戴手套，避免与皮肤接触。
2.实验过程中如遇到有毒或者刺激性物质及有害物质产生，必要时实验操作需要手套箱内完成以免对实验人员造成伤害
3.实验后产生的废弃物需分类存储，并交于专业生物废气物处理公司处理，以免造成环境污染Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.
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| 产品说明 | 3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)是一种有效的 S-腺苷高半胱氨酸水解酶 的抑制剂,Ki值是3.9μM. |
| Introduction | 3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)is an inhibitor of Sdenosylhomocysteine hydrolase, with aKiof 3.9 μM; 3eazaadenosine has antinflammatory, antiroliferative and antiIVactivity. |
| Application1 | 3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)具有抗炎,抗增殖,抗HIV等活性 |
| Application2 | |
| Application3 |
3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)药理学：
3-Deazaadenosine (hydrochloride) 是一种 S-腺苷高半胱氨酸水解酶 (S-adenosylhomocysteine hydrolase) 抑制剂，Ki 值为 3.9 µM；3-Deazaadenosine (hydrochloride) 具有抗炎、抗增殖、抗 HIV 等活性。
3-Deazaadenosine (hydrochloride) 是一种 S-腺苷高半胱氨酸水解酶 (S-adenosylhomocysteine hydrolase) 抑制剂，Ki 值为 3.9 µM；3-Deazaadenosine (hydrochloride) 具有抗炎、抗增殖、抗 HIV 等活性。
| 警示图 | |
| 危险性 | warning |
| 危险性警示 | Not available |
| 安全声明 | H303吞入可能有害+H313皮肤接触可能有害+H2413吸入可能对身体有害 |
| 安全防护 | P264处理后彻底清洗+P280戴防护手套/穿防护服/戴防护眼罩/戴防护面具+P305如果进入眼睛+P351用水小心冲洗几分钟+P338取出隐形眼镜（如果有）并且易于操作,继续冲洗+P337如果眼睛刺激持续+P2393获得医疗建议/护理 |
| 备注 | 实验过程中防止吸入、食入，做好安全防护 |
| Gordon RK, et al. Anti-HIV-1 activity of 3-deaza-adenosine analogs. Inhibition of S-adenosylhomocysteine hydrolase and nucleotide congeners. Eur J Biochem. 2003 Sep;270(17):3507-17. |
| Jeong SY, et al. 3-deazaadenosine, a S-adenosylhomocysteine hydrolase inhibitor, has dual effects on NF-kappaB regulation. Inhibition of NF-kappaB transcriptional activity and promotion of IkappaBalph |
| Sedding DG, et al. 3-Deazaadenosine prevents smooth muscle cell proliferation and neointima formation by interfering with Ras signaling. Circ Res. 2009 May 22;104(10):1192-200. |
3-脱氮腺苷盐酸盐(86583-19-9,3-Deazaadenosine hydrochloride)参考文献：
1、Anti-HIV-1 activity of 3-deaza-adenosine analogs. Inhibition of S-adenosylhomocysteine hydrolase and nucleotide congeners
Richard K Gordon 1, Krzysztof Ginalski, Witold R Rudnicki, Leszek Rychlewski, Marvin C Pankaskie, Janusz M Bujnicki, Peter K Chiang
Abstract Eight adenosine analogs, 3-deaza-adenosine (DZA), 3-deaza-(+/-)aristeromycin (DZAri), 2',3'-dideoxy-adenosine (ddAdo), 2',3'-dideoxy-3-deaza-adenosine (ddDZA), 2',3'-dideoxy-3-deaza-(+/-)aristeromycin (ddDZAri), 3-deaza-5'-(+/-)noraristeromycin (DZNAri), 3-deaza-neplanocin A (DZNep), and neplanocin A (NepA), were tested as inhibitors of human placenta S-adenosylhomocysteine (AdoHcy) hydrolase. The order of potency for the inhibition of human placental AdoHcy hydrolase was: DZNep approximately NepA >> DZAri approximately DZNAri > DZA >> ddAdo approximately ddDZA approximately ddDZAri. These same analogs were examined for their anti-HIV-1 activities measured by the reduction in p24 antigen produced by 3'-azido-3'-deoxythymidine (AZT)-sensitive HIV-1 isolates, A012 and A018, in phytohemagglutinin-stimulated peripheral blood mononuclear (PBMCs) cells. Interestingly, DZNAri and the 2',3'-dideoxy 3-deaza-nucleosides (ddAdo, ddDZAri, and ddDZA) were only marginal inhibitors of p24 antigen production in HIV-1 infected PBMC. DZNAri is unique because it is the only DZA analog with a deleted methylene group that precludes anabolic phosphorylation. In contrast, the other analogs were potent inhibitors of p24 antigen production by both HIV-1 isolates. Thus it was postulated that these nucleoside analogs could exert their antiviral effect via a combination of anabolically generated nucleotides (with the exception of DZNAri), which could inhibit reverse transcriptase or other viral enzymes, and the inhibition of viral or cellular methylation reactions. Additionally, QSAR-like models based on the molecular mechanics (MM) were developed to predict the order of potency of eight adenosine analogs for the inhibition of human AdoHcy hydrolase. In view of the potent antiviral activities of the DZA analogs, this approach provides a promising tool for designing and screening of more potent AdoHcy hydrolase inhibitors and antiviral agents.
2、3-deazaadenosine, a S-adenosylhomocysteine hydrolase inhibitor, has dual effects on NF-kappaB regulation. Inhibition of NF-kappaB transcriptional activity and promotion of IkappaBalpha degradation
S Y Jeong 1, S G Ahn, J H Lee, H S Kim, J W Kim, H Rhim, S W Jeong, I K Kim
Abstract Previously we reported that 3-deazaadenosine (DZA), a potent inhibitor and substrate for S-adenosylhomocysteine hydrolase inhibits bacterial lipopolysaccharide-induced transcription of tumor necrosis factor-alpha and interleukin-1beta in mouse macrophage RAW 264.7 cells. In this study, we demonstrate the effects of DZA on nuclear factor-kappaB (NF-kappaB) regulation. DZA inhibits the transcriptional activity of NF-kappaB through the hindrance of p65 (Rel-A) phosphorylation without reduction of its nuclear translocation and DNA binding activity. The inhibitory effect of DZA on NF-kappaB transcriptional activity is potentiated by the addition of homocysteine. Taken together, DZA promotes the proteolytic degradation of IkappaBalpha, but not IkappaBbeta, resulting in an increase of DNA binding activity of NF-kappaB in the nucleus in the absence of its transcriptional activity in RAW 264.7 cells. The reduction of IkappaBalpha by DZA is neither involved in IkappaB kinase complex activation nor modulated by the addition of homocysteine. This study strongly suggests that DZA may be a potent drug for the treatment of diseases in which NF-kappaB plays a central pathogenic role, as well as a useful tool for studying the regulation and physiological functions of NF-kappaB.
3、3-Deazaadenosine prevents smooth muscle cell proliferation and neointima formation by interfering with Ras signaling
Daniel G Sedding 1, Monique Tröbs, Fabian Reich, Gerhard Walker, Ludger Fink, Werner Haberbosch, Wigbert Rau, Harald Tillmanns, Klaus T Preissner, Rainer M Bohle, Alexander C Langheinrich
Abstract 3-Deazaadenosine (c3Ado) is a potent inhibitor of S-adenosylhomocysteine hydrolase, which regulates cellular methyltransferase activity. In the present study, we sought to determine the effect of c3Ado on vascular smooth muscle cell (VSMC) function and neointima formation in vivo. c3Ado dose-dependently prevented the proliferation and migration of human coronary VSMCs in vitro. This was accompanied by an increased expression of the cyclin-dependent kinase inhibitors p21(WAF1/Cip1), p27(Kip1), a decreased expression of G(1)/S phase cyclins, and a lack of retinoblastoma protein hyperphosphorylation. In accordance with these findings, fluorescence-activated cell-sorting analysis of propidium iodide-stained cells indicated a cell cycle arrest in the G(0)/G(1) phase. Importantly, c3Ado did not affect the number of viable (trypan blue exclusion) or apoptotic cells (TUNEL). Mechanistically, c3Ado prevented FCS-induced Ras carboxyl methylation and membrane translocation and activity by inhibiting isoprenylcysteine carboxyl methyltransferase and reduced FCS-induced extracellular signal-regulated kinase (ERK)1/2 and Akt phosphorylation in a dose-dependent manner. Conversely, rescuing signal transduction by overexpression of a constitutive active Ras mutant abrogated c3Ado's effect on proliferation. For in vivo studies, the femoral artery of C57BL/6 mice was dilated and mice were fed a diet containing 150 microg of c3Ado per day. c3Ado prevented dilation-induced Ras activation, as well as ERK1/2 and Akt phosphorylation in vivo. At day 21, VSMC proliferation (proliferating-cell nuclear antigen [PCNA]-positive cells), as well as the neointima/media ratio (0.7+/-0.2 versus 1.6+/-0.4; P<0.05) were significantly reduced, without any changes in the number of apoptotic cells. Our data indicate that c3Ado interferes with Ras methylation and function and thereby with mitogenic activation of ERK1/2 and Akt, preventing VSMC cell cycle entry and proliferation and neointima formation in vivo. Thus, therapeutic inhibition of S-adenosylhomocysteine hydrolase by c3Ado may represent a save and effective novel approach to prevent vascular proliferative disease.
1、Anti-HIV-1 activity of 3-deaza-adenosine analogs. Inhibition of S-adenosylhomocysteine hydrolase and nucleotide congeners
Richard K Gordon 1, Krzysztof Ginalski, Witold R Rudnicki, Leszek Rychlewski, Marvin C Pankaskie, Janusz M Bujnicki, Peter K Chiang
Abstract Eight adenosine analogs, 3-deaza-adenosine (DZA), 3-deaza-(+/-)aristeromycin (DZAri), 2',3'-dideoxy-adenosine (ddAdo), 2',3'-dideoxy-3-deaza-adenosine (ddDZA), 2',3'-dideoxy-3-deaza-(+/-)aristeromycin (ddDZAri), 3-deaza-5'-(+/-)noraristeromycin (DZNAri), 3-deaza-neplanocin A (DZNep), and neplanocin A (NepA), were tested as inhibitors of human placenta S-adenosylhomocysteine (AdoHcy) hydrolase. The order of potency for the inhibition of human placental AdoHcy hydrolase was: DZNep approximately NepA >> DZAri approximately DZNAri > DZA >> ddAdo approximately ddDZA approximately ddDZAri. These same analogs were examined for their anti-HIV-1 activities measured by the reduction in p24 antigen produced by 3'-azido-3'-deoxythymidine (AZT)-sensitive HIV-1 isolates, A012 and A018, in phytohemagglutinin-stimulated peripheral blood mononuclear (PBMCs) cells. Interestingly, DZNAri and the 2',3'-dideoxy 3-deaza-nucleosides (ddAdo, ddDZAri, and ddDZA) were only marginal inhibitors of p24 antigen production in HIV-1 infected PBMC. DZNAri is unique because it is the only DZA analog with a deleted methylene group that precludes anabolic phosphorylation. In contrast, the other analogs were potent inhibitors of p24 antigen production by both HIV-1 isolates. Thus it was postulated that these nucleoside analogs could exert their antiviral effect via a combination of anabolically generated nucleotides (with the exception of DZNAri), which could inhibit reverse transcriptase or other viral enzymes, and the inhibition of viral or cellular methylation reactions. Additionally, QSAR-like models based on the molecular mechanics (MM) were developed to predict the order of potency of eight adenosine analogs for the inhibition of human AdoHcy hydrolase. In view of the potent antiviral activities of the DZA analogs, this approach provides a promising tool for designing and screening of more potent AdoHcy hydrolase inhibitors and antiviral agents.
2、3-deazaadenosine, a S-adenosylhomocysteine hydrolase inhibitor, has dual effects on NF-kappaB regulation. Inhibition of NF-kappaB transcriptional activity and promotion of IkappaBalpha degradation
S Y Jeong 1, S G Ahn, J H Lee, H S Kim, J W Kim, H Rhim, S W Jeong, I K Kim
Abstract Previously we reported that 3-deazaadenosine (DZA), a potent inhibitor and substrate for S-adenosylhomocysteine hydrolase inhibits bacterial lipopolysaccharide-induced transcription of tumor necrosis factor-alpha and interleukin-1beta in mouse macrophage RAW 264.7 cells. In this study, we demonstrate the effects of DZA on nuclear factor-kappaB (NF-kappaB) regulation. DZA inhibits the transcriptional activity of NF-kappaB through the hindrance of p65 (Rel-A) phosphorylation without reduction of its nuclear translocation and DNA binding activity. The inhibitory effect of DZA on NF-kappaB transcriptional activity is potentiated by the addition of homocysteine. Taken together, DZA promotes the proteolytic degradation of IkappaBalpha, but not IkappaBbeta, resulting in an increase of DNA binding activity of NF-kappaB in the nucleus in the absence of its transcriptional activity in RAW 264.7 cells. The reduction of IkappaBalpha by DZA is neither involved in IkappaB kinase complex activation nor modulated by the addition of homocysteine. This study strongly suggests that DZA may be a potent drug for the treatment of diseases in which NF-kappaB plays a central pathogenic role, as well as a useful tool for studying the regulation and physiological functions of NF-kappaB.
3、3-Deazaadenosine prevents smooth muscle cell proliferation and neointima formation by interfering with Ras signaling
Daniel G Sedding 1, Monique Tröbs, Fabian Reich, Gerhard Walker, Ludger Fink, Werner Haberbosch, Wigbert Rau, Harald Tillmanns, Klaus T Preissner, Rainer M Bohle, Alexander C Langheinrich
Abstract 3-Deazaadenosine (c3Ado) is a potent inhibitor of S-adenosylhomocysteine hydrolase, which regulates cellular methyltransferase activity. In the present study, we sought to determine the effect of c3Ado on vascular smooth muscle cell (VSMC) function and neointima formation in vivo. c3Ado dose-dependently prevented the proliferation and migration of human coronary VSMCs in vitro. This was accompanied by an increased expression of the cyclin-dependent kinase inhibitors p21(WAF1/Cip1), p27(Kip1), a decreased expression of G(1)/S phase cyclins, and a lack of retinoblastoma protein hyperphosphorylation. In accordance with these findings, fluorescence-activated cell-sorting analysis of propidium iodide-stained cells indicated a cell cycle arrest in the G(0)/G(1) phase. Importantly, c3Ado did not affect the number of viable (trypan blue exclusion) or apoptotic cells (TUNEL). Mechanistically, c3Ado prevented FCS-induced Ras carboxyl methylation and membrane translocation and activity by inhibiting isoprenylcysteine carboxyl methyltransferase and reduced FCS-induced extracellular signal-regulated kinase (ERK)1/2 and Akt phosphorylation in a dose-dependent manner. Conversely, rescuing signal transduction by overexpression of a constitutive active Ras mutant abrogated c3Ado's effect on proliferation. For in vivo studies, the femoral artery of C57BL/6 mice was dilated and mice were fed a diet containing 150 microg of c3Ado per day. c3Ado prevented dilation-induced Ras activation, as well as ERK1/2 and Akt phosphorylation in vivo. At day 21, VSMC proliferation (proliferating-cell nuclear antigen [PCNA]-positive cells), as well as the neointima/media ratio (0.7+/-0.2 versus 1.6+/-0.4; P<0.05) were significantly reduced, without any changes in the number of apoptotic cells. Our data indicate that c3Ado interferes with Ras methylation and function and thereby with mitogenic activation of ERK1/2 and Akt, preventing VSMC cell cycle entry and proliferation and neointima formation in vivo. Thus, therapeutic inhibition of S-adenosylhomocysteine hydrolase by c3Ado may represent a save and effective novel approach to prevent vascular proliferative disease.
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