购物车 
-
加地基莫德
- names：
Gardiquimod diTFA
- CAS号：
1159840-61-5
MDL Number： MFCD31619251 - MF(分子式)： C21H25F6N5O5 MW(分子量)： 541.44
- EINECS: Reaxys Number:
- Pubchem ID:44592365 Brand:BIOFOUNT
加地基莫德(1159840-61-5,Gardiquimod diTFA)是一种咪唑啉类似物，TLR7/8 激动剂。Gardiquimod diTFA 可抑制巨噬细胞和活化外周血单个核细胞 (PBMCs) 的 HIV-1 感染。当浓度低于 10 μM 时，Gardiquimod diTFA 特别激活 TLR7。
| 货品编码 | 规格 | 纯度 | 价格 (¥) | 现价(¥) | 特价(¥) | 库存描述 | 数量 | 总计 (¥) |
|---|---|---|---|---|---|---|---|---|
| YZM000638-10mg | 10mg | 99.28% | ¥ 891.00 | ¥ 891.00 | 2-3天 | ¥ 0.00 | ||
| YZM000638-5mg | 5mg | 99.28% | ¥ 536.25 | ¥ 536.25 | 2-3天 | ¥ 0.00 |
| 中文别名 | 加地基莫德(1159840-61-5);加地基莫德TFA盐;加地喹莫特三氟乙酸盐;加替莫德三氟乙酸盐;加地基莫德;加迪基莫德;加地莫特三氟乙酸盐;加洛地莫三氟乙酸酯; |
| 英文别名 | Gardiquimod diTFA(1159840-61-5);Gardiquimod trifluoroacetate;Gardiquimodtrifluoroacetate;1H-Imidazo[4,5-c]quinoline-1-ethanol,4-amino-2-[(ethylamino)methyl]-α,α-dChemicalbookimethyl-,2,2,2-trifluoroacetate(1:2);gardiquimodTFAsalt;GardiquimodTFA;GARDIQUIMODTFA;GardiquimoddiTFA; |
| CAS号 | 1159840-61-5 |
| SMILES | OC(C)(C)CN1C(CNCC)=NC2=C1C3=CC=CC=C3N=C2N.FC(C(O)=O)(F)F.FC(C(O)=O)(F)F |
| Inchi | InChI=1S/C17H23N5O.2C2HF3O2/c1-4-19-9-13-21-14-15(22(13)10-17(2,3)23)11-7-5-6-8-12(11)20-16(14)18;2*3-2(4,5)1(6)7/h5-8,19,23H,4,9-10H2,1-3H3,(H2,18,20);2*(H,6,7) |
| InchiKey | XFQPQSJDMJVOBN-UHFFFAOYSA-N |
| 分子式 Formula | C21H25F6N5O5 |
| 分子量 Molecular Weight | 541.44 |
| 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100 mg/mL(184.69 mM;Need ultrasonic)H2O : 25 mg/mL(46.17 mM;Need ultrasonic) |
| 性状 | 固体粉末,Power |
| 储藏条件 Storage conditions | 干燥，黑暗，短期（几天至几周）在0-4 C，长期（几个月至几年）在-20C。如果保存正确，则> 2年 |
加地基莫德(1159840-61-5,Gardiquimod diTFA)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 | 加地基莫德(1159840-61-5,Gardiquimod diTFA)是一个特异的TLR7激动剂，也能抑制HIV-1逆转录酶 |
| Introduction | 加地基莫德(1159840-61-5,Gardiquimod diTFA)is a specificTLR7agonist which can also inhibitHIV reverse transcriptase. |
| Application1 | |
| Application2 | |
| Application3 |
加地基莫德(1159840-61-5,Gardiquimod diTFA)药理学：
1、Gardiquimod diTFA 可抑制巨噬细胞和活化分裂血核细胞（PBMCs）的HIV-1感染。当浓度降低10μM时，Gardiquimod diTFA特别是，Gardiquimod diTFA ，一种咪唑啉类似物，TLR7 / 8激动剂。激活TLR7。
2、加地基莫德是一种化合物，可选择性地作用于小鼠和人类形式的收费型受体7（TLR7）。它起免疫反应调节剂的作用。核心结构是1H-咪唑并[4,5-c]喹啉，如咪喹莫特和瑞西莫德等相关药物中发现的。它在结构上与雷西莫德非常相似，区别仅在于用氧气进行氮气转换。
1、Gardiquimod diTFA 可抑制巨噬细胞和活化分裂血核细胞（PBMCs）的HIV-1感染。当浓度降低10μM时，Gardiquimod diTFA特别是，Gardiquimod diTFA ，一种咪唑啉类似物，TLR7 / 8激动剂。激活TLR7。
2、加地基莫德是一种化合物，可选择性地作用于小鼠和人类形式的收费型受体7（TLR7）。它起免疫反应调节剂的作用。核心结构是1H-咪唑并[4,5-c]喹啉，如咪喹莫特和瑞西莫德等相关药物中发现的。它在结构上与雷西莫德非常相似，区别仅在于用氧气进行氮气转换。
| 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 |
| Buitendijk M, et al. Gardiquimod: a Toll-like receptor-7 agonist that inhibits HIV type 1 infection of human macrophages and activated T cells. AIDS Res Hum Retroviruses. 2013 Jun;29(6):907-18. |
| Ma F, et al. The TLR7 agonists imiquimod and gardiquimod improve DC-based immunotherapy for melanoma in mice. Cell Mol Immunol. 2010 Sep;7(5):381-8. |
| Zhou Z, et al. TLR7/8 agonists promote NK-DC cross-talk to enhance NK cell anti-tumor effects in hepatocellular carcinoma. Cancer Lett. 2015 Dec 28;369(2):298-306. |
| Guo S, Zhang Y, Wang Z, Yu Y, Wang G. Intraperitoneal gardiquimod protects against hepatotoxicity through inhibition of oxidative stress and inflammation in mice with sepsis. J Biochem Mol Toxicol. 20 |
| Jia B, Luo X, Cheng FW, Li L, Hu DJ, Wang F, Zhang SQ. Gardiquimod inhibits the expression of calcium-induced differentiation markers in HaCaT cells. Mol Biol Rep. 2013 Nov;40(11):6363-9. doi: 10.1007 |
加地基莫德(1159840-61-5,Gardiquimod diTFA)参考文献：
1、Gardiquimod: a Toll-like receptor-7 agonist that inhibits HIV type 1 infection of human macrophages and activated T cells
Maarten Buitendijk 1, Susan K Eszterhas, Alexandra L Howell
Abstract Immune response modifiers are being studied as therapeutic agents for viral infections and cancer. These molecules include agonists for the Toll-like receptors (TLR), a family of innate immune receptors. TLR7 and 8, located in cellular endosomes, bind single-stranded RNA characteristic of viral genomes, and trigger intracellular signaling pathways that induce inflammatory cytokines and antiviral innate immune factors. We studied the anti-HIV-1 effects of gardiquimod, a specific TLR7 agonist when used at concentrations below 10 μM, in macrophages and activated peripheral blood mononuclear cells (PBMCs). Gardiquimod, added prior to or within 2 days after infection with X4, R5, or dual-tropic (R5/X4) strains of HIV-1, significantly reduced infection in these cells. Cocultures of activated PBMCs added to gardiquimod-treated and HIV-1-exposed macrophages demonstrated minimal HIV-1 replication for up to 10 days, suggesting that gardiquimod inhibited activated PBMCs viral amplification from HIV-1-exposed macrophages. Gardiquimod treatment of both activated PBMCs and macrophages induced interferon-alpha (IFN-α) transcription within hours of addition, and sustained IFN-α protein secretion for several days. Treatment of cells with a peptide inhibitor to the MyD88 adaptor protein blocked the induction of IFN-α by gardiquimod, and partially reversed the anti-HIV effects in activated PBMCs. Blocking the IFN-α receptor with a neutralizing antibody also reduced the anti-HIV effect of gardiquimod. Gardiquimod inhibited HIV-1 reverse transcriptase, an early step in the life cycle of HIV-1. These findings suggest that gardiquimod, functioning as both an immune system modifier and a reverse transcriptase inhibitor, could be developed as a novel therapeutic agent to block systemic and mucosal transmission of HIV-1.
2、The TLR7 agonists imiquimod and gardiquimod improve DC-based immunotherapy for melanoma in mice
Fang Ma 1, Jianhua Zhang, Jian Zhang, Cai Zhang
Abstract Toll-like receptors (TLRs) are a family of highly conserved germline-encoded pattern-recognition receptors that are essential for host immune responses. TLR ligands represent a promising class of immunotherapeutics or vaccine adjuvants with the potential to generate an effective antitumor immune response. The TLR7/8 agonists have aroused interest because they not only activate antigen-presenting cells but also promote activation of T and natural killer (NK) cells. However, the exact mechanism by which stimulation of these TLRs promotes immune responses remains unclear, and different TLR7/8 agonists have been found to induce different responses. In this study, we demonstrate that both gardiquimod and imiquimod promote the proliferation of murine splenocytes, stimulate the activation of splenic T, NK and natural killer T (NKT) cells, increase the cytolytic activity of splenocytes against B16 and MCA-38 tumor cell lines, and enhance the expression of costimulatory molecules and IL-12 by macrophages and bone marrow-derived dendritic cells (DCs). In a murine model, both agonists improved the antitumor effects of tumor lysate-loaded DCs, resulting in delayed growth of subcutaneous B16 melanoma tumors and suppression of pulmonary metastasis. Further, we found that gardiquimod demonstrated more potent antitumor activity than imiquimod. These results suggest that TLR7/8 agonists may serve as potent innate and adaptive immune response modifiers in tumor therapy. More importantly, they can be used as vaccine adjuvants to potentiate the efficiency of DC-based tumor immunotherapy.
3、TLR7/8 agonists promote NK-DC cross-talk to enhance NK cell anti-tumor effects in hepatocellular carcinoma
Zhixia Zhou 1, Xin Yu 1, Jian Zhang 1, Zhigang Tian 2, Cai Zhang
Abstract Hepatocellular carcinoma (HCC) is a common cancer worldwide and the third leading cause of cancer death. Immunotherapy is considered a promising treatment with the aim to boost or arouse HCC-specific immune responses. TLR7 and TLR8 agonists are effective immunomodulators and have been applied topically for the treatment of certain skin tumors and viral infections. Here, we explored the role of TLR7 and TLR8 agonists on the activation of dendritic cells (DCs) and natural killer (NK) cells. We demonstrated that these agonists could directly activate NK cells, promoting the maturation of immature DCs. Meanwhile, DCs also assisted in the function of NK cells, resulting in enhanced anti-tumor immune responses to HCC. Importantly, the combination therapy with NK cells stimulated with DCs and TLR7/8 agonist Gardiquimod (GDQ) significantly suppresses the growth of human HepG2 liver carcinoma xenografts. This study provides a new immunotherapeutic approach for human HCC based on DC-NK cross-talk and also suggests that TLR7 and/or TLR8 agonists, particularly GDQ, may serve as potent innate and adaptive immune response immunomodulators in tumor therapy.
1、Gardiquimod: a Toll-like receptor-7 agonist that inhibits HIV type 1 infection of human macrophages and activated T cells
Maarten Buitendijk 1, Susan K Eszterhas, Alexandra L Howell
Abstract Immune response modifiers are being studied as therapeutic agents for viral infections and cancer. These molecules include agonists for the Toll-like receptors (TLR), a family of innate immune receptors. TLR7 and 8, located in cellular endosomes, bind single-stranded RNA characteristic of viral genomes, and trigger intracellular signaling pathways that induce inflammatory cytokines and antiviral innate immune factors. We studied the anti-HIV-1 effects of gardiquimod, a specific TLR7 agonist when used at concentrations below 10 μM, in macrophages and activated peripheral blood mononuclear cells (PBMCs). Gardiquimod, added prior to or within 2 days after infection with X4, R5, or dual-tropic (R5/X4) strains of HIV-1, significantly reduced infection in these cells. Cocultures of activated PBMCs added to gardiquimod-treated and HIV-1-exposed macrophages demonstrated minimal HIV-1 replication for up to 10 days, suggesting that gardiquimod inhibited activated PBMCs viral amplification from HIV-1-exposed macrophages. Gardiquimod treatment of both activated PBMCs and macrophages induced interferon-alpha (IFN-α) transcription within hours of addition, and sustained IFN-α protein secretion for several days. Treatment of cells with a peptide inhibitor to the MyD88 adaptor protein blocked the induction of IFN-α by gardiquimod, and partially reversed the anti-HIV effects in activated PBMCs. Blocking the IFN-α receptor with a neutralizing antibody also reduced the anti-HIV effect of gardiquimod. Gardiquimod inhibited HIV-1 reverse transcriptase, an early step in the life cycle of HIV-1. These findings suggest that gardiquimod, functioning as both an immune system modifier and a reverse transcriptase inhibitor, could be developed as a novel therapeutic agent to block systemic and mucosal transmission of HIV-1.
2、The TLR7 agonists imiquimod and gardiquimod improve DC-based immunotherapy for melanoma in mice
Fang Ma 1, Jianhua Zhang, Jian Zhang, Cai Zhang
Abstract Toll-like receptors (TLRs) are a family of highly conserved germline-encoded pattern-recognition receptors that are essential for host immune responses. TLR ligands represent a promising class of immunotherapeutics or vaccine adjuvants with the potential to generate an effective antitumor immune response. The TLR7/8 agonists have aroused interest because they not only activate antigen-presenting cells but also promote activation of T and natural killer (NK) cells. However, the exact mechanism by which stimulation of these TLRs promotes immune responses remains unclear, and different TLR7/8 agonists have been found to induce different responses. In this study, we demonstrate that both gardiquimod and imiquimod promote the proliferation of murine splenocytes, stimulate the activation of splenic T, NK and natural killer T (NKT) cells, increase the cytolytic activity of splenocytes against B16 and MCA-38 tumor cell lines, and enhance the expression of costimulatory molecules and IL-12 by macrophages and bone marrow-derived dendritic cells (DCs). In a murine model, both agonists improved the antitumor effects of tumor lysate-loaded DCs, resulting in delayed growth of subcutaneous B16 melanoma tumors and suppression of pulmonary metastasis. Further, we found that gardiquimod demonstrated more potent antitumor activity than imiquimod. These results suggest that TLR7/8 agonists may serve as potent innate and adaptive immune response modifiers in tumor therapy. More importantly, they can be used as vaccine adjuvants to potentiate the efficiency of DC-based tumor immunotherapy.
3、TLR7/8 agonists promote NK-DC cross-talk to enhance NK cell anti-tumor effects in hepatocellular carcinoma
Zhixia Zhou 1, Xin Yu 1, Jian Zhang 1, Zhigang Tian 2, Cai Zhang
Abstract Hepatocellular carcinoma (HCC) is a common cancer worldwide and the third leading cause of cancer death. Immunotherapy is considered a promising treatment with the aim to boost or arouse HCC-specific immune responses. TLR7 and TLR8 agonists are effective immunomodulators and have been applied topically for the treatment of certain skin tumors and viral infections. Here, we explored the role of TLR7 and TLR8 agonists on the activation of dendritic cells (DCs) and natural killer (NK) cells. We demonstrated that these agonists could directly activate NK cells, promoting the maturation of immature DCs. Meanwhile, DCs also assisted in the function of NK cells, resulting in enhanced anti-tumor immune responses to HCC. Importantly, the combination therapy with NK cells stimulated with DCs and TLR7/8 agonist Gardiquimod (GDQ) significantly suppresses the growth of human HepG2 liver carcinoma xenografts. This study provides a new immunotherapeutic approach for human HCC based on DC-NK cross-talk and also suggests that TLR7 and/or TLR8 agonists, particularly GDQ, may serve as potent innate and adaptive immune response immunomodulators in tumor therapy.
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