LAS17 is a potent and selective tyrosine-directed irreversible inhibitor for glutathione S-Transferase Pi (GSTP1) [1]. LAS17 inhibits GSTP1 activity with an IC50 of 0.5 µM[2].
体外研究 (In Vitro)
Glutathione S-Transferase Pi (GSTP1) mediates cellular defense against reactive electrophiles. LAS17 inhibits GSTP1 activity in vitro in a concentration-dependent manner[1]. LAS17 (10 µM; Serum-free survival 48 h) treatment in 231MFP breast cancer cells recapitulates the serum-free cell survival impairments observed with genetic inactivation of GSTP1[2]. GSTP1 knockdown in LAS17 (10 µM) treatment in 231MFP cells results in increased levels of phosphorylated AMPK and acetyl CoA carboxylase (ACC)[2]. LAS17 treatment in 231MFP cells also shows reduced levels of ATP, lactic acid, purine nucleotides, and diacylated phospholipids and alkylacyl ether lipids and increased levels of acyl carnitines (ACs), ceramides, lysophospholipids[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
231MFP breast cancer cells
Concentration:
10 µM
Incubation Time:
48 hours
Result:
Recapitulated the serum-free cell survival impairments observed with genetic inactivation of GSTP1.
Western Blot Analysis[2]
Cell Line:
231MFP cells
Concentration:
10 µM
Incubation Time:
Result:
LAS17-treated 231MFP cells show increased levels of phosphorylated AMPK and ACC.
体内研究 (In Vivo)
Daily administration of LAS17 (20 mg/kg ip, once per day) significantly impairs 231MFP breast tumor xenograft growth in immune-deficient mice when treatment is initiated 2 days after subcutaneous injection of cells, and LAS17 even slows tumor growth when initiated 16 days after tumor implantation, with no observable toxicity and no weight-change[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Severe combined immunodeficiency (SCID) mice bearing 231MFP tumor xenograft[2]
Dosage:
20 mg/kg (prepared in PBS:ethanol:PEG40 (18:1:1))
Administration:
Daily administration i.p., once per day
Result:
Significantly impaired 231MFP breast tumor xenograft growth.
分子量
359.25
Formula
C15H20Cl2N4O2
CAS 号
2362527-67-9
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. L A Crawford, et al. A tyrosine-reactive irreversible inhibitor for glutathione S-transferase Pi (GSTP1). Mol Biosyst. 2016 May 24;12(6):1768-71.
[2]. Sharon M Louie, et al. GSTP1 Is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity. Cell Chem Biol. 2016 May 19;23(5):567-578.
LAS17 is a potent and selective tyrosine-directed irreversible inhibitor for glutathione S-Transferase Pi (GSTP1) [1]. LAS17 inhibits GSTP1 activity with an IC50 of 0.5 µM[2].
体外研究 (In Vitro)
Glutathione S-Transferase Pi (GSTP1) mediates cellular defense against reactive electrophiles. LAS17 inhibits GSTP1 activity in vitro in a concentration-dependent manner[1]. LAS17 (10 µM; Serum-free survival 48 h) treatment in 231MFP breast cancer cells recapitulates the serum-free cell survival impairments observed with genetic inactivation of GSTP1[2]. GSTP1 knockdown in LAS17 (10 µM) treatment in 231MFP cells results in increased levels of phosphorylated AMPK and acetyl CoA carboxylase (ACC)[2]. LAS17 treatment in 231MFP cells also shows reduced levels of ATP, lactic acid, purine nucleotides, and diacylated phospholipids and alkylacyl ether lipids and increased levels of acyl carnitines (ACs), ceramides, lysophospholipids[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
231MFP breast cancer cells
Concentration:
10 µM
Incubation Time:
48 hours
Result:
Recapitulated the serum-free cell survival impairments observed with genetic inactivation of GSTP1.
Western Blot Analysis[2]
Cell Line:
231MFP cells
Concentration:
10 µM
Incubation Time:
Result:
LAS17-treated 231MFP cells show increased levels of phosphorylated AMPK and ACC.
体内研究 (In Vivo)
Daily administration of LAS17 (20 mg/kg ip, once per day) significantly impairs 231MFP breast tumor xenograft growth in immune-deficient mice when treatment is initiated 2 days after subcutaneous injection of cells, and LAS17 even slows tumor growth when initiated 16 days after tumor implantation, with no observable toxicity and no weight-change[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Severe combined immunodeficiency (SCID) mice bearing 231MFP tumor xenograft[2]
Dosage:
20 mg/kg (prepared in PBS:ethanol:PEG40 (18:1:1))
Administration:
Daily administration i.p., once per day
Result:
Significantly impaired 231MFP breast tumor xenograft growth.
分子量
359.25
Formula
C15H20Cl2N4O2
CAS 号
2362527-67-9
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. L A Crawford, et al. A tyrosine-reactive irreversible inhibitor for glutathione S-transferase Pi (GSTP1). Mol Biosyst. 2016 May 24;12(6):1768-71.
[2]. Sharon M Louie, et al. GSTP1 Is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity. Cell Chem Biol. 2016 May 19;23(5):567-578.
LAS17 is a potent and selective tyrosine-directed irreversible inhibitor for glutathione S-Transferase Pi (GSTP1) [1]. LAS17 inhibits GSTP1 activity with an IC50 of 0.5 µM[2].
体外研究 (In Vitro)
Glutathione S-Transferase Pi (GSTP1) mediates cellular defense against reactive electrophiles. LAS17 inhibits GSTP1 activity in vitro in a concentration-dependent manner[1]. LAS17 (10 µM; Serum-free survival 48 h) treatment in 231MFP breast cancer cells recapitulates the serum-free cell survival impairments observed with genetic inactivation of GSTP1[2]. GSTP1 knockdown in LAS17 (10 µM) treatment in 231MFP cells results in increased levels of phosphorylated AMPK and acetyl CoA carboxylase (ACC)[2]. LAS17 treatment in 231MFP cells also shows reduced levels of ATP, lactic acid, purine nucleotides, and diacylated phospholipids and alkylacyl ether lipids and increased levels of acyl carnitines (ACs), ceramides, lysophospholipids[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
231MFP breast cancer cells
Concentration:
10 µM
Incubation Time:
48 hours
Result:
Recapitulated the serum-free cell survival impairments observed with genetic inactivation of GSTP1.
Western Blot Analysis[2]
Cell Line:
231MFP cells
Concentration:
10 µM
Incubation Time:
Result:
LAS17-treated 231MFP cells show increased levels of phosphorylated AMPK and ACC.
体内研究 (In Vivo)
Daily administration of LAS17 (20 mg/kg ip, once per day) significantly impairs 231MFP breast tumor xenograft growth in immune-deficient mice when treatment is initiated 2 days after subcutaneous injection of cells, and LAS17 even slows tumor growth when initiated 16 days after tumor implantation, with no observable toxicity and no weight-change[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Severe combined immunodeficiency (SCID) mice bearing 231MFP tumor xenograft[2]
Dosage:
20 mg/kg (prepared in PBS:ethanol:PEG40 (18:1:1))
Administration:
Daily administration i.p., once per day
Result:
Significantly impaired 231MFP breast tumor xenograft growth.
分子量
359.25
Formula
C15H20Cl2N4O2
CAS 号
2362527-67-9
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. L A Crawford, et al. A tyrosine-reactive irreversible inhibitor for glutathione S-transferase Pi (GSTP1). Mol Biosyst. 2016 May 24;12(6):1768-71.
[2]. Sharon M Louie, et al. GSTP1 Is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity. Cell Chem Biol. 2016 May 19;23(5):567-578.
NBDHEX is a potent glutathione S-transferase P1-1 (GSTP1-1) inhibitor. NBDHEX induces apoptosis of tumor cells. NBDHEX acts as an anticancer agent by inhibiting GSTs catalytic activity, avoiding inconvenience of the inhibitor extrusion from the cell by specific pumps and disrupting the interaction between the GSTP1-1 and key signaling effectors. NBDHEX can also act as late-phase autophagy inhibitor[1][2].
NBDHEX (0.05-20 μM; 48 hours; H69 and H69AR cells) is cytotoxic toward cell lung cancer H69 and H69AR cells[2]. NBDHEX (0-5 μM; 24 hours; H69AR cells) treatment results in a dose-dependent apoptosis in the H69AR cell line[2]. NBDHEX (3 μM; 1-12 hours; H69AR cells) treatment increases the phosphorylation of JNK/c-Jun in H69AR cells in a time-dependent fashion[2]. NBDHEX treatment shows a marked increase in phosphorylation of p38MAPK, and also increases GSSG content in a time-dependent manner in H69 cells[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
H69 and H69AR cells
Concentration:
0.05-20 μM
Incubation Time:
48 hours
Result:
The dose-response profiles revealed a good cytotoxic activity both in sensitive H69 cell line (LC50 of 2.3 μM) and in its Adriamycin-resistant counterpart H69AR (LC50 of 4.5 μM).
Apoptosis Analysis[2]
Cell Line:
H69AR cells
Concentration:
0 μM, 0.5 μM, 1 μM, 2 μM, 3 μM, 4 μM, 5 μM
Incubation Time:
24 hours
Result:
Resulted in a dose-dependent apoptosis in the H69AR cell line.
Western Blot Analysis[2]
Cell Line:
H69AR cells
Concentration:
3 μM
Incubation Time:
1 hour,3 hours, 6 hours, 12 hours
Result:
Increased the phosphorylation of JNK/c-Jun in H69AR cells in a time-dependent fashion.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Sha HH, et al. 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio) hexanol: a promising new anticancer compound. Biosci Rep. 2018 Feb 13;38(1). pii: BSR20171440.
[2]. Filomeni G, et al. 6-(7-Nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol, a specific glutathione S-transferase inhibitor, overcomes the multidrug resistance (MDR)-associated protein 1-mediated MDR in small cell lung cancer. Mol Cancer Ther. 2008 Feb;7(2):371-9.
[3]. Pellizzari Tregno F, et al. In vitro and in vivo efficacy of 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol (NBDHEX) on human melanoma. Eur J Cancer. 2009 Sep;45(14):2606-17.
NBDHEX is a potent glutathione S-transferase P1-1 (GSTP1-1) inhibitor. NBDHEX induces apoptosis of tumor cells. NBDHEX acts as an anticancer agent by inhibiting GSTs catalytic activity, avoiding inconvenience of the inhibitor extrusion from the cell by specific pumps and disrupting the interaction between the GSTP1-1 and key signaling effectors. NBDHEX can also act as late-phase autophagy inhibitor[1][2].
NBDHEX (0.05-20 μM; 48 hours; H69 and H69AR cells) is cytotoxic toward cell lung cancer H69 and H69AR cells[2]. NBDHEX (0-5 μM; 24 hours; H69AR cells) treatment results in a dose-dependent apoptosis in the H69AR cell line[2]. NBDHEX (3 μM; 1-12 hours; H69AR cells) treatment increases the phosphorylation of JNK/c-Jun in H69AR cells in a time-dependent fashion[2]. NBDHEX treatment shows a marked increase in phosphorylation of p38MAPK, and also increases GSSG content in a time-dependent manner in H69 cells[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
H69 and H69AR cells
Concentration:
0.05-20 μM
Incubation Time:
48 hours
Result:
The dose-response profiles revealed a good cytotoxic activity both in sensitive H69 cell line (LC50 of 2.3 μM) and in its Adriamycin-resistant counterpart H69AR (LC50 of 4.5 μM).
Apoptosis Analysis[2]
Cell Line:
H69AR cells
Concentration:
0 μM, 0.5 μM, 1 μM, 2 μM, 3 μM, 4 μM, 5 μM
Incubation Time:
24 hours
Result:
Resulted in a dose-dependent apoptosis in the H69AR cell line.
Western Blot Analysis[2]
Cell Line:
H69AR cells
Concentration:
3 μM
Incubation Time:
1 hour,3 hours, 6 hours, 12 hours
Result:
Increased the phosphorylation of JNK/c-Jun in H69AR cells in a time-dependent fashion.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Sha HH, et al. 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio) hexanol: a promising new anticancer compound. Biosci Rep. 2018 Feb 13;38(1). pii: BSR20171440.
[2]. Filomeni G, et al. 6-(7-Nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol, a specific glutathione S-transferase inhibitor, overcomes the multidrug resistance (MDR)-associated protein 1-mediated MDR in small cell lung cancer. Mol Cancer Ther. 2008 Feb;7(2):371-9.
[3]. Pellizzari Tregno F, et al. In vitro and in vivo efficacy of 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol (NBDHEX) on human melanoma. Eur J Cancer. 2009 Sep;45(14):2606-17.