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Tariquidar
別名: XR9576
Tariquidar是一種有效的，選擇性的，非競爭性P-glycoprotein抑制劑，在CHrB30細胞系中Kd為5.1 nM，作用于MDR細胞系逆轉(zhuǎn)耐藥性。Phase 3。
Tariquidar Chemical Structure
CAS: 206873-63-4
產(chǎn)品質(zhì)控
批次：
純度：
99.81%
99.81
Tariquidar相關(guān)產(chǎn)品
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|---|---|---|
| 相關(guān)化合物庫 | FDA藥物庫 天然產(chǎn)物庫 離子通道配體庫 外泌體分泌相關(guān)化合物庫 鈣通道阻滯劑庫 | 點擊展開 |
相關(guān)信號通路圖
細胞實驗數(shù)據(jù)示例
| 細胞系 | 實驗類型 | 給藥濃度 | 孵育時間 | 活性描述 | 文獻信息 |
|---|---|---|---|---|---|
| SW620 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human SW620 cells assessed as cell viability after 48 hrs by MTT assay, IC50=25μM | 26197160 | |
| HepG2 | Function assay | 10 uM | 90 mins | Inhibition of P-gp mediated efflux in adriamycin-resistant human HepG2 cells assessed as intracellular rhodamine-123 accumulation at 10 uM incubated in dark condition for 90 mins by flow cytometry relative to control | 27328029 |
| MDCK | Function assay | 30 mins | Activity at BCRP (unknown origin) expressed in MDCK cells using rhodamine 123 as substrate incubated for 30 mins prior to substrate addition measured after 30 mins by fluorometric analysis, EC50=0.01μM | 23374872 | |
| OVCAR8 | Function assay | 1000 nM | 72 hrs | Potentiation of cytotoxicity against human OVCAR8 cells assessed as IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 8.53 +/- 1.95 nM), IC50=0.00518μM | 27504669 |
| K562/A02 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human K562/A02 cells after 48 hrs by MTT assay, IC50=27.19μM | 28645831 | |
| Kb-V1 | Function assay | 10 mins | Inhibition of ABCB1 expressed in Kb-V1 cells after 10 mins by calcein-AM assay, IC50=0.223μM | 21570282 | |
| KBv1 | Function assay | Inhibition of ABCB1 overexpressed in human KBv1 cells by flow cytometric-based calcein-AM efflux assay, IC50=0.223μM | 19170519 | ||
| KBV1 | Function assay | Inhibition of ABCB1 in human KBV1 cells assessed as inhibition of calcein-AM efflux, IC50=0.22μM | 26774038 | ||
| A2780 | Function assay | 30 mins | Inhibition of human Pgp in A2780 cells after 30 mins by Hoechst 33342 assay, IC50=0.12589μM | 18083034 | |
| KB-3-1 | Function assay | 1000 nM | 72 hrs | Potentiation of doxorubicin-induced cytotoxicity against human KB-3-1 cells assessed as doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 0.15 +/- 0.04 uM), IC50=0.11μM | 27504669 |
| OVCAR8 | Function assay | 1000 nM | 72 hrs | Potentiation of doxorubicin-induced cytotoxicity against human OVCAR8 cells assessed as doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 0.12 +/- 0.03 uM), IC50=0.08μM | 27504669 |
| A2780/ADR | Function assay | Inhibition of P-glycoprotein-mediated multidrug resistance in adriamycin-resistant human A2780/ADR cells by calcein AM assay, IC50=0.078μM | 19250834 | ||
| A2780adr | Function assay | Inhibition of P-gp expressed in A2780adr cells by calcein AM accumulation assay, IC50=0.08μM | 21354800 | ||
| A2780 | Function assay | Inhibition of P-gp in human adriamycin-resistant A2780 cells by Hoechst 33342 assay, IC50=0.07244μM | 18678495 | ||
| KBV1 | Function assay | 1000 nM | 72 hrs | Inhibition of human ABCB1 expressed in KBV1 cells assessed as potentiation of doxorubicin-induced cytotoxicity by measuring doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 5.07 +/- 0.19 uM), IC50=0.07μM | 27504669 |
| CEM/VLB500 | Function assay | 3 days | Reversal of P-gp-mediated multidrug resistance to in human CEM/VLB500 cells after 3 days by resazurin assay, EC50=0.068μM | 17399990 | |
| EMT6/AR1.0 | Function assay | 1 hr | Inhibition of mouse Pgp in EMT6/AR1.0 cells after 1 hr by daunorubicin accumulation assay, IC50=0.06457μM | 18083034 | |
| EMT6/AR1.0 | Function assay | 1 hr | Inhibition of mouse Pgp in EMT6/AR1.0 cells after 1 hr by daunorubicin accumulation assay, IC50=0.064μM | 18083034 | |
| MDCK | Function assay | 30 mins | Inhibition of P-glycoprotein (unknown origin) expressed in MDCK cells assessed as reduction of calcein-AM transport after 30 mins by fluorescence assay, EC50=0.044μM | 24607999 | |
| MDCK | Function assay | 30 mins | Activity at MDR1 (unknown origin) expressed in MDCK cells using calcein AM as substrate incubated for 30 mins prior to substrate addition measured after 30 mins by fluorometric analysis, EC50=0.044μM | 23374872 | |
| NCI-ADR-RES | Function assay | 1000 nM | 72 hrs | Inhibition of human ABCB1 expressed in NCI-ADR-RES cells assessed as potentiation of cytotoxicity by measuring IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 3714.80 +/- 383.58 nM), IC50=0.01851μM | 27504669 |
| KBV1 | Function assay | 1000 nM | 72 hrs | Inhibition of human ABCB1 expressed in KBV1 cells assessed as potentiation of cytotoxicity by measuring IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 277.68 +/- 56.61 nM), IC50=0.00066μM | 27504669 |
| KBV1 | Function assay | 10 mins | Inhibition of ABCB1 in human KBV1 cells after 10 mins by Calcein-AM microplate assay, IC50=0.223μM | 24900683 | |
| MCF7/Topo | Function assay | Inhibition of ABCG2 overexpressed in human MCF7/Topo cells by flow cytometric-based mitoxantrone efflux assay, IC50=0.916μM | 19170519 | ||
| MCF7/Topo | Function assay | 2 hrs | Inhibition of ABCG2 in human MCF7/Topo cells after 2 hrs by Hoechst 33342 staining based fluorescence assay, IC50=0.526μM | 30128080 | |
| MCF7/Topo | Function assay | 2 hrs | Inhibition of ABCG2 in human MCF7/Topo cells after 2 hrs by Hoechst 33342 microplate assay, IC50=0.526μM | 24900683 | |
| MCF7/Topo | Function assay | Inhibition of ABCG2 expressed in human MCF7/Topo cells by Hoechst microplate assay, IC50=0.526μM | 21570282 | ||
| MCF7/Topo | Function assay | Inhibition of ABCG2 in human MCF7/Topo cells by Hoechst 33342 assay, IC50=0.52μM | 26774038 | ||
| K562/A02 | Function assay | 48 hrs | Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 measured after 48 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=1.6μM | 28645831 | |
| MCF-7 MX | Function assay | Inhibition of BCRP expressed in MCF-7 MX cells using Hoechst 33342 staining, IC50=1.5μM | 21354800 | ||
| MCF7 | Function assay | Inhibition of ABCG2 in human mitoxantrone-resistant MCF7 cells by Hoechst 33342 assay, IC50=1.44544μM | 18678495 | ||
| HFE | Cytotoxicity assay | 72 hrs | Cytotoxicity against human HFE cells assessed as cell viability after 72 hrs by MTT assay, IC50=1.28μM | 26197160 | |
| MDCK | Function assay | Inhibition of BCRP expressed in MDCK cells using Hoechst 33342 staining, IC50=0.94μM | 21354800 | ||
| KBV | Function assay | 5 uM | 72 hrs | Reversal of P-gp-mediated drug resistance in human KBV cells assessed as potentiation of cytotoxicity by measuring IC50 at 5 uM after 72 hrs by MTT assay (Rvb = 398.34 +/- 0.58 uM), IC50=5.24μM | 30384042 |
| K562/A02 | Function assay | 48 hrs | Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured after 6 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=4.97μM | 28645831 | |
| KBV | Function assay | 10 uM | 72 hrs | Reversal of P-gp-mediated drug resistance in human KBV cells assessed as potentiation of cytotoxicity by measuring IC50 at 10 uM after 72 hrs by MTT assay (Rvb = 398.34 +/- 0.58 uM), IC50=4.46μM | 30384042 |
| K562/A02 | Function assay | 48 hrs | Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured immediately by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=3.02μM | 28645831 | |
| K562/A02 | Function assay | 5 uM | 48 hrs | Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 at 5 uM measured after 48 hrs by MTT assay (Rvb = 43.75 to 96.91 uM), IC50=1.97μM | 28645831 |
| CCRF-CEM/VCR1000 | Function assay | 240 secs | Inhibition of P-glycoprotein-mediated daunorubicin efflux from human CCRF-CEM/VCR1000 cells after 240 secs by FACS flow cytometric analysis, IC50=0.03311μM | 22452412 | |
| MDCK | Function assay | Inhibition of MDR1 expressed in MDCK cells using rhodamine 123 staining by flow cytometry, IC50=0.21μM | 21354800 | ||
| NCI-ADR-RES | Function assay | 1000 nM | 72 hrs | Inhibition of human ABCB1 expressed in NCI-ADR-RES cells assessed as potentiation of doxorubicin-induced cytotoxicity by measuring doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 5.54 +/- 0.60 uM), IC50=0.24μM | 27504669 |
| MCF7 MX | Function assay | Inhibition of BCRP expressed in MCF7 MX cells by Hoechst 33342 staining, IC50=0.68μM | 19932960 | ||
| MDCK | Function assay | Inhibition of BCRP expressed in MDCK cells by pheophorbide A assay, IC50=0.85μM | 19932960 | ||
| K562/A02 | Function assay | 48 hrs | Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured after 24 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=14.39μM | 28645831 | |
| K562/A02 | Function assay | 48 hrs | Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured after 12 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=8.28μM | 28645831 | |
| CCD-18Co | Cytotoxicity assay | 48 hrs | Cytotoxicity against human CCD-18Co cells assessed as cell viability after 48 hrs by MTT assay, IC50=25μM | 26197160 | |
| SW620/AD300 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human SW620/AD300 cells assessed as cell viability after 48 hrs by MTT assay, IC50=25μM | 26197160 | |
| HLF | Cytotoxicity assay | 48 hrs | Cytotoxicity against HLF cells assessed as inhibition of cell proliferation after 48 hrs by MTT assay, IC50=16.69μM | 27328029 | |
| CEM/VLB500 | Growth inhibition assay | 3 days | Growth inhibition of human CEM/VLB500 cells after 3 days by resazurin assay, GI50=13.5μM | 17399990 | |
| A2780adr | Function assay | 10 uM | 30 mins | Inhibition of ABCB1 in human A2780adr cells assessed as increase in accumulation of calcein AM at 10 uM preincubated for 30 mins followed by calcein AM addition measured every 60 secs for 60 mins by fluorescence assay relative to control | 29547272 |
| K562/A02 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human K562/A02 cells overexpressing P-gp assessed as reduction in cell viability after 48 hrs by MTT assay, IC50=27.19μM | 29631786 | |
| K562 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human K562 cells after 48 hrs by MTT assay, IC50=31.56μM | 28645831 | |
| SK-N-MC | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells | 29435139 | ||
| KB-V1 | Function assay | 200 nM | Inhibition of P-gp in human KB-V1 cells assessed as increase in rhodamine 123 accumulation at 200 nM | 21657271 | |
| NB1643 | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells | 29435139 | ||
| SK-N-SH | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells | 29435139 | ||
| HEK293 | Function assay | 1000 nM | 72 hrs | Potentiation of doxorubicin-induced cytotoxicity against HEK293 cells assessed as doxorubicin IC50 at 1000 nM after 72 hrs by CCK8 assay (Rvb = 5.28 +/- 0.74 nM), IC50=0.00495μM | 27504669 |
| KB-3-1 | Function assay | 1000 nM | 72 hrs | Potentiation of cytotoxicity against human KB-3-1 cells assessed as IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 0.78 +/- 0.27 nM), IC50=0.00041μM | 27504669 |
| HEK293 | Function assay | 1000 nM | 72 hrs | Inhibition of human ABCB1 transfected in HEK293 cells assessed as potentiation of doxorubicin-induced cytotoxicity by measuring doxorubicin IC50 at 1000 nM after 72 hrs by CCK8 assay (Rvb = 504.65 +/- 44.94 nM), IC50=0.02477μM | 27504669 |
| HCT116 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human HCT116 cells assessed as cell viability after 48 hrs by MTT assay, IC50=12.5μM | 26197160 | |
| MCF7/ADR | Cytotoxicity assay | 48 hrs | Intrinsic cytotoxicity against human MCF7/ADR cells assessed as inhibition of cell proliferation after 48 hrs by MTT assay, IC50=13.1μM | 27328029 | |
| K562 | Cytotoxicity assay | 48 hrs | Cytotoxicity against human K562 cells assessed as reduction in cell viability after 48 hrs by MTT assay, IC50=31.56μM | 29631786 | |
| HepG2 | Cytotoxicity assay | 48 hrs | Cytotoxicity against adriamycin-resistant human HepG2 cells assessed as inhibition of cell proliferation after 48 hrs by MTT assay, IC50=37.2μM | 27328029 | |
| K562/DOX | Function assay | 1 uM | 10 mins | Inhibition of P-gp in human K562/DOX cells assessed as increase in rhodamine-123 efflux in human K562 cells at 1 uM incubated for 10 mins hrs by flow cytometry relative to untreated control | 28113128 |
| 點擊查看更多細胞系數(shù)據(jù) | |||||
生物活性
| 產(chǎn)品描述 | Tariquidar是一種有效的，選擇性的，非競爭性P-glycoprotein抑制劑，在CHrB30細胞系中Kd為5.1 nM，作用于MDR細胞系逆轉(zhuǎn)耐藥性。Phase 3。 | ||
|---|---|---|---|
| 靶點 |
|
| 體外研究(In Vitro) | ||||
| 體外研究活性 | Tariquidar高親和力結(jié)合到P-gp，Bmax為275 pmol/mg。Tariquidar與P-gp底物非競爭性地相互作用。Tariquidar作用于CHrB30 細胞，增加這些細胞毒素的穩(wěn)態(tài)積累，達到非P-gp表達的AuxB1細胞中觀察的水平，EC50為487 nM。Tariquidar可以抑制 P-gp的對Vanadate敏感的ATPase活性，抑制達 60-70%,有效IC50值為43 nM。[1]Tariquidar高濃度時，可以抑制其他耐藥機制。1 μM Tariquidar在體外，可以廢除ABCG2（BCRP）介導的Camptothecins耐藥性。[2]Tariquidar增強幾種藥物的細胞毒性，包括Doxorubicin。處理具有內(nèi)在耐藥性的小鼠結(jié)腸癌細胞系MC26，Doxorubicin比0.1 μM Tariquidar (36 vs 7 nM)的IC50值低5倍。處理具有獲得性化療抗性的小鼠乳腺癌，人類小細胞肺癌，和和人類卵巢癌細胞系(EMT6/AR1.0, H69/LX4 和 2780 AD)，Doxorubicin 比0.1 μM Tariquidar的IC50值低22-150倍。從培養(yǎng)系統(tǒng)除去Tariquidar后，P-gp的抑制作用持續(xù)23小時。[3]Tariquidar恢復(fù)Doxorubicin作用于MCF7WT乳腺癌細胞系衍生的多細胞腫瘤球體模型的細胞毒性。[4] |
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|---|---|---|---|---|
| 激酶實驗 | 穩(wěn)態(tài)藥物累積實驗 | |||
| 細胞在37°C下5% CO2環(huán)境中溫育60分鐘，達到穩(wěn)態(tài)，反應(yīng)體積為1 mL。在10-9-10-6 M濃度范圍內(nèi) 調(diào)查調(diào)節(jié)劑XR9576對[3H]-配體累積的影響。DMSO儲存液中加入調(diào)節(jié)劑，最終溶劑濃度為0.2 %(v/v)。細胞收集后，通過液體閃爍計數(shù)和歸一化細胞蛋白質(zhì)含量測量累計的藥物。 | ||||
| 細胞實驗 | 細胞系 | 小鼠乳腺癌細胞系MDR EMT6/AR1.0 | ||
| 濃度 | ~100 nM Tariquidar | |||
| 孵育時間 | 4 天 | |||
| 方法 | 細胞按每孔800個接種在含100 μL 培養(yǎng)基的96孔板中，在37°C下溫育4小時。隨后加入不同濃度的調(diào)節(jié)劑或溶劑對照（50μL/孔），再溫育1小時，加入細胞毒性藥物。加入細胞毒性藥物（50μL），每孔按一式四份得到終濃度的范圍。再溫育4天 ,通過Sulforhodamine B實驗測評貼壁細胞的細胞增殖。 |
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| 實驗圖片 | 檢測方法 | 檢測指標 | 實驗圖片 | PMID |
| Immunofluorescence | MRP7 |
|
23393594 | |
| 體內(nèi)研究(In Vivo) | ||
| 體內(nèi)研究活性 | Tariquidar(2-8 mg/kg 口服處理)顯著增強Doxorubicin(5 mg/kg, 靜脈注射)處理MC26小鼠結(jié)腸癌的抗腫瘤活性。Tariquidar和XR9576(6-12 mg/kg 口服處理)合用共處理人類移植瘤， 完全恢復(fù)作用于兩個高度抗MDR的人類移植瘤(2780AD, H69/LX4)的抗腫瘤活性。[3] |
|
|---|---|---|
| 動物實驗 | Animal Models | 攜帶結(jié)腸癌移植瘤MC26的小鼠 |
| Dosages | 8 mg/kg | |
| Administration | Tariquidar (口服處理)和Doxorubicin (5 mg/kg,靜脈注射）共處理 | |
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT01663545 | Completed | Epilepsies Partial |
National Institute of Neurological Disorders and Stroke (NINDS)|National Institutes of Health Clinical Center (CC) |
July 31 2012 | -- |
| NCT01547754 | Terminated | HIV-Associated Cognitive Motor Complex |
National Institute of Mental Health (NIMH)|National Institutes of Health Clinical Center (CC) |
January 9 2012 | -- |
| NCT01386476 | Completed | Drug Resistance |
National Institute of Mental Health (NIMH)|National Institutes of Health Clinical Center (CC) |
June 15 2011 | -- |
| NCT00082368 | Completed | Cancer |
National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) |
May 16 2004 | Phase 2 |
化學信息&溶解度
| 分子量 | 646.73 | 分子式 | C38H38N4O6 |
| CAS號 | 206873-63-4 | SDF | Download Tariquidar SDF |
| Smiles | COC1=C(C=C2CN(CCC2=C1)CCC3=CC=C(C=C3)NC(=O)C4=CC(=C(C=C4NC(=O)C5=CC6=CC=CC=C6N=C5)OC)OC)OC | ||
| 儲存條件(自收到貨起) | |||
|
體外溶解度 |
DMSO : 8 mg/mL ( (12.36 mM) ；DMSO吸濕會降低化合物溶解度，請使用新開封DMSO) Water : Insoluble Ethanol : Insoluble |
摩爾濃度計算器 |
|
體內(nèi)溶解度 現(xiàn)配現(xiàn)用，請按從左到右的順序依次添加，澄清后再加入下一溶劑 |
動物體內(nèi)配方計算器 | ||||
實驗計算
動物體內(nèi)配方計算器（澄清溶液）
第一步：請輸入基本實驗信息（考慮到實驗過程中的損耗，建議多配一只動物的藥量）
mg/kg
g
μL
只
第二步：請輸入動物體內(nèi)配方組成（配方適用于不溶于水的藥物；不同批次藥物配方比例不同，請聯(lián)系Selleck為您提供正確的澄清溶液配方）
% DMSO
%
% Tween 80
% ddH2O
%DMSO
%
計算結(jié)果：
工作液濃度： mg/ml；
DMSO母液配制方法： mg 藥物溶于μL DMSO溶液（母液濃度mg/mL，注：如該濃度超過該批次藥物DMSO溶解度，請先聯(lián)系Selleck）；
體內(nèi)配方配制方法：取μL DMSO母液，加入μL PEG300，混勻澄清后加入μL Tween 80，混勻澄清后加入μL ddH2O，混勻澄清。
體內(nèi)配方配制方法：取μL DMSO母液，加入μL Corn oil，混勻澄清。
注意：1. 首先保證母液是澄清的；
2.一定要按照順序依次將溶劑加入，進行下一步操作之前必須保證上一步操作得到的是澄清的溶液，可采用渦旋、超聲或水浴加熱等物理方法助溶。
技術(shù)支持
在訂購、運輸、儲存和使用我們的產(chǎn)品的任何階段，您遇到的任何問題，均可以通過撥打我們的熱線電話400-668-6834，或者技術(shù)支持郵箱tech@selleck.cn，直接聯(lián)系到我們。我們會在24小時內(nèi)盡快聯(lián)系您。
如果有其他問題，請給我們留言。
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常見問題及建議解決方法
問題 1:
Can you please give me more specific and detailed information of how to dissolve and use this compound (S8028) for in vivo studies?
回答：
Tariquidar in 30% Propylene glycol, 5% Tween 80, 65% D5W at 30mg/ml will be a suspension or emulsion. If you are going to administrate the compound by oral gavage, it is fine. We also have test some vehicles for Tariquidar for i.p injection, and it is soluble in 5% DMSO+45% PEG 300+ddH2O at 2mg/ml clearly. When preparing the solution, please dissolve the compound in DMSO clearly first, then add PEG. After they mixed well, then dilute with water.
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