購物車 
-
3-脫氮腺苷鹽酸鹽
- names：
3-Deazaadenosine hydrochloride
- CAS號：
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-脫氮腺苷鹽酸鹽(86583-19-9,3-Deazaadenosine hydrochloride)是一種S-腺苷高半胱氨酸水解酶（S-adenosylhomocysteine hydrolase）抑制劑，Ki 約為3.9 µM； 3-脫氮雜腺苷鹽酸鹽（鹽酸鹽）具有抗炎，抗增殖，抗HIV等活性。
| 貨品編碼 | 規格 | 純度 | 價格 (￥) | 現價(￥) | 特價(￥) | 庫存描述 | 數量 | 總計 (￥) |
|---|---|---|---|---|---|---|---|---|
| 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 |
| 中文別名 | 3-脫氮腺苷鹽酸鹽(86583-19-9);3-脫氮腺苷;鹽酸3-脫氮腺苷;鹽酸3-脫氮腺苷;3-去氮雜腺苷（鹽酸鹽);HY-W013332A;CS-0069568; |
| 英文別名 | 3-Deazaadenosine hydrochloride(86583-19-9);3-deazaadenosine;3-deazaadenosine hydrochloride;3-deazaadenosine hydrochloride;3-Deazaadenosine (hydrochloride):HY-W013332A;CS-0069568; |
| CAS號 | 86583-19-9 |
| 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 |
| 溶解度Solubility | 生物體外In Vitro:DMSO溶解度41.67 mg/mL(137.66 mM;Need ultrasonic) |
| 性狀 | Solid |
| 儲藏條件 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-脫氮腺苷鹽酸鹽(86583-19-9,3-Deazaadenosine hydrochloride)實驗注意事項：
1.實驗前需戴好防護眼鏡，穿戴防護服和口罩，佩戴手套，避免與皮膚接觸。
2.實驗過程中如遇到有毒或者刺激性物質及有害物質產生，必要時實驗操作需要手套箱內完成以免對實驗人員造成傷害
3.實驗后產生的廢棄物需分類存儲，并交于專業生物廢氣物處理公司處理，以免造成環境污染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.
Tags:3-脫氮腺苷鹽酸鹽試劑,3-脫氮腺苷鹽酸鹽雜質,3-脫氮腺苷鹽酸鹽中間體,3-脫氮腺苷鹽酸鹽合成,3-脫氮腺苷鹽酸鹽密度,3-脫氮腺苷鹽酸鹽溶解度,3-脫氮腺苷鹽酸鹽旋光度,3-脫氮腺苷鹽酸鹽閃點,3-脫氮腺苷鹽酸鹽熔點,3-脫氮腺苷鹽酸鹽購買,
| 產品說明 | 3-脫氮腺苷鹽酸鹽(86583-19-9,3-Deazaadenosine hydrochloride)是一種有效的 S-腺苷高半胱氨酸水解酶 的抑制劑,Ki值是3.9μM. |
| Introduction | 3-脫氮腺苷鹽酸鹽(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-脫氮腺苷鹽酸鹽(86583-19-9,3-Deazaadenosine hydrochloride)具有抗炎,抗增殖,抗HIV等活性 |
| Application2 | |
| Application3 |
3-脫氮腺苷鹽酸鹽(86583-19-9,3-Deazaadenosine hydrochloride)藥理學：
3-Deazaadenosine (hydrochloride) 是一種 S-腺苷高半胱氨酸水解酶 (S-adenosylhomocysteine hydrolase) 抑制劑，Ki 值為 3.9 µM；3-Deazaadenosine (hydrochloride) 具有抗炎、抗增殖、抗 HIV 等活性。
3-Deazaadenosine (hydrochloride) 是一種 S-腺苷高半胱氨酸水解酶 (S-adenosylhomocysteine hydrolase) 抑制劑，Ki 值為 3.9 µM；3-Deazaadenosine (hydrochloride) 具有抗炎、抗增殖、抗 HIV 等活性。
| 警示圖 | |
| 危險性 | warning |
| 危險性警示 | Not available |
| 安全聲明 | H303吞入可能有害+H313皮膚接觸可能有害+H2413吸入可能對身體有害 |
| 安全防護 | P264處理后徹底清洗+P280戴防護手套/穿防護服/戴防護眼罩/戴防護面具+P305如果進入眼睛+P351用水小心沖洗幾分鐘+P338取出隱形眼鏡（如果有）并且易于操作,繼續沖洗+P337如果眼睛刺激持續+P2393獲得醫療建議/護理 |
| 備注 | 實驗過程中防止吸入、食入，做好安全防護 |
| 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-脫氮腺苷鹽酸鹽(86583-19-9,3-Deazaadenosine hydrochloride)參考文獻：
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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