購物車 
-
加地基莫德
- names：
Gardiquimod diTFA
- CAS號：
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)是一種咪唑啉類似物，TLR7/8 激動劑。Gardiquimod diTFA 可抑制巨噬細胞和活化外周血單個核細胞 (PBMCs) 的 HIV-1 感染。當濃度低于 10 μM 時，Gardiquimod diTFA 特別激活 TLR7。
| 貨品編碼 | 規格 | 純度 | 價格 (￥) | 現價(￥) | 特價(￥) | 庫存描述 | 數量 | 總計 (￥) |
|---|---|---|---|---|---|---|---|---|
| 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 |
| 中文別名 | 加地基莫德(1159840-61-5);加地基莫德TFA鹽;加地喹莫特三氟乙酸鹽;加替莫德三氟乙酸鹽;加地基莫德;加迪基莫德;加地莫特三氟乙酸鹽;加洛地莫三氟乙酸酯; |
| 英文別名 | 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號 | 1159840-61-5 |
| 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 |
| 溶解度Solubility | 生物體外In Vitro:DMSO溶解度100 mg/mL(184.69 mM;Need ultrasonic)H2O : 25 mg/mL(46.17 mM;Need ultrasonic) |
| 性狀 | 固體粉末,Power |
| 儲藏條件 Storage conditions | 干燥，黑暗，短期（幾天至幾周）在0-4 C，長期（幾個月至幾年）在-20C。如果保存正確，則> 2年 |
加地基莫德(1159840-61-5,Gardiquimod diTFA)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.
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| 產品說明 | 加地基莫德(1159840-61-5,Gardiquimod diTFA)是一個特異的TLR7激動劑，也能抑制HIV-1逆轉錄酶 |
| 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)藥理學：
1、Gardiquimod diTFA 可抑制巨噬細胞和活化分裂血核細胞（PBMCs）的HIV-1感染。當濃度降低10μM時，Gardiquimod diTFA特別是，Gardiquimod diTFA ，一種咪唑啉類似物，TLR7 / 8激動劑。激活TLR7。
2、加地基莫德是一種化合物，可選擇性地作用于小鼠和人類形式的收費型受體7（TLR7）。它起免疫反應調節劑的作用。核心結構是1H-咪唑并[4,5-c]喹啉，如咪喹莫特和瑞西莫德等相關藥物中發現的。它在結構上與雷西莫德非常相似，區別僅在于用氧氣進行氮氣轉換。
1、Gardiquimod diTFA 可抑制巨噬細胞和活化分裂血核細胞（PBMCs）的HIV-1感染。當濃度降低10μM時，Gardiquimod diTFA特別是，Gardiquimod diTFA ，一種咪唑啉類似物，TLR7 / 8激動劑。激活TLR7。
2、加地基莫德是一種化合物，可選擇性地作用于小鼠和人類形式的收費型受體7（TLR7）。它起免疫反應調節劑的作用。核心結構是1H-咪唑并[4,5-c]喹啉，如咪喹莫特和瑞西莫德等相關藥物中發現的。它在結構上與雷西莫德非常相似，區別僅在于用氧氣進行氮氣轉換。
| 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 |
| 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)參考文獻：
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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