Alectinib-d6 is deuterium labeled Alectinib. Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
488.65
Formula
C30H28D6N4O2
CAS 号
1616374-19-6
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[3]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
Alectinib (0-1000 nM; 2 hours; NCI-H2228 cells) treatment could prevent autophosphorylation of ALK in NCI-H2228 cells expressing EML4-ALK, and it also resulted in substantial suppression of phosphorylation of STAT3 and AKT[1]. Alectinib (0-1000 nM; 5 days; HCC827, A549, or NCIH522 cells) treatment reduces cell activity in a dose-dependent manner[1].
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.
Western Blot Analysis[1]
Cell Line:
NCI-H2228 cells
Concentration:
0 nM,10 nM,100 nM, 1000 nM
Incubation Time:
2 hours
Result:
Inhibition of ALK phosphorylation and signal transduction.
Cell Viability Assay[1]
Cell Line:
HCC827, A549, or NCIH522 cells
Concentration:
0-1000 nM
Incubation Time:
5 days
Result:
Reduced cell activity in a dose-dependent manner.
体内研究 (In Vivo)
Alectinib (0.2-20 mg/kg; oral administration; once daily; for 11 days; SCID or nude mice bearing NCI-H2228 cells) treatment can result in dose-dependent tumor growth inhibition (EC50 of 0.46 mg/kg) and tumor regression. At any dose level, no differences in body weight or gross signs of toxicity are observed[1].
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:
SCID or nude mice bearing NCI-H2228 cells[1]
Dosage:
0.2 mg/kg, 0.6 mg/kg, 2 mg/kg, 6 mg/kg, 20 mg/kg
Administration:
Oral administration; once daily; for 11 days
Result:
Resulted in dose-dependent tumor growth inhibition (EC50 of 0.46 mg/kg) and tumor regression.
Clinical Trial
分子量
482.62
Formula
C30H34N4O2
CAS 号
1256580-46-7
中文名称
艾乐替尼；阿雷替尼
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[2]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
Alectinib Hydrochloride (CH5424802 Hydrochloride; RO5424802 Hydrochloride; AF-802 Hydrochloride) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
Alectinib (0-1000 nM; 2 hours; NCI-H2228 cells) treatment could prevent autophosphorylation of ALK in NCI-H2228 cells expressing EML4-ALK, and it also resulted in substantial suppression of phosphorylation of STAT3 and AKT[1]. Alectinib (0-1000 nM; 5 days; HCC827, A549, or NCIH522 cells) treatment reduces cell activity in a dose-dependent manner[1].
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.
Western Blot Analysis[1]
Cell Line:
NCI-H2228 cells
Concentration:
0 nM,10 nM,100 nM, 1000 nM
Incubation Time:
2 hours
Result:
Inhibition of ALK phosphorylation and signal transduction.
Cell Viability Assay[1]
Cell Line:
HCC827, A549, or NCIH522 cells
Concentration:
0-1000 nM
Incubation Time:
5 days
Result:
Reduced cell activity in a dose-dependent manner.
体内研究 (In Vivo)
Alectinib (0.2-20 mg/kg; oral administration; once daily; for 11 days; SCID or nude mice bearing NCI-H2228 cells) treatment can result in dose-dependent tumor growth inhibition (EC50 of 0.46 mg/kg) and tumor regression. At any dose level, no differences in body weight or gross signs of toxicity are observed[1].
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:
SCID or nude mice bearing NCI-H2228 cells[1]
Dosage:
0.2 mg/kg, 0.6 mg/kg, 2 mg/kg, 6 mg/kg, 20 mg/kg
Administration:
Oral administration; once daily; for 11 days
Result:
Resulted in dose-dependent tumor growth inhibition (EC50 of 0.46 mg/kg) and tumor regression.
Clinical Trial
分子量
519.08
Formula
C30H35ClN4O2
CAS 号
1256589-74-8
中文名称
艾乐替尼盐酸盐；盐酸阿雷替尼
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[2]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
Alectinib Hydrochloride (CH5424802 Hydrochloride; RO5424802 Hydrochloride; AF-802 Hydrochloride) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
Alectinib (0-1000 nM; 2 hours; NCI-H2228 cells) treatment could prevent autophosphorylation of ALK in NCI-H2228 cells expressing EML4-ALK, and it also resulted in substantial suppression of phosphorylation of STAT3 and AKT[1]. Alectinib (0-1000 nM; 5 days; HCC827, A549, or NCIH522 cells) treatment reduces cell activity in a dose-dependent manner[1].
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.
Western Blot Analysis[1]
Cell Line:
NCI-H2228 cells
Concentration:
0 nM,10 nM,100 nM, 1000 nM
Incubation Time:
2 hours
Result:
Inhibition of ALK phosphorylation and signal transduction.
Cell Viability Assay[1]
Cell Line:
HCC827, A549, or NCIH522 cells
Concentration:
0-1000 nM
Incubation Time:
5 days
Result:
Reduced cell activity in a dose-dependent manner.
体内研究 (In Vivo)
Alectinib (0.2-20 mg/kg; oral administration; once daily; for 11 days; SCID or nude mice bearing NCI-H2228 cells) treatment can result in dose-dependent tumor growth inhibition (EC50 of 0.46 mg/kg) and tumor regression. At any dose level, no differences in body weight or gross signs of toxicity are observed[1].
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:
SCID or nude mice bearing NCI-H2228 cells[1]
Dosage:
0.2 mg/kg, 0.6 mg/kg, 2 mg/kg, 6 mg/kg, 20 mg/kg
Administration:
Oral administration; once daily; for 11 days
Result:
Resulted in dose-dependent tumor growth inhibition (EC50 of 0.46 mg/kg) and tumor regression.
Clinical Trial
分子量
519.08
Formula
C30H35ClN4O2
CAS 号
1256589-74-8
中文名称
艾乐替尼盐酸盐；盐酸阿雷替尼
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[2]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
Alectinib-d8 (CH5424802-d8) is the deuterium labeled Alectinib. Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
490.67
Formula
C30H26D8N4O2
CAS 号
1256585-15-5
中文名称
艾乐替尼 d8
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[3]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
Alectinib-d8 (CH5424802-d8) is the deuterium labeled Alectinib. Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
490.67
Formula
C30H26D8N4O2
CAS 号
1256585-15-5
中文名称
艾乐替尼 d8
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[3]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
Alectinib-d8 (CH5424802-d8) is the deuterium labeled Alectinib. Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM (in an ATP-competitive manner), and also inhibits ALK F1174L and ALK R1275Q with IC50s of 1 nM and 3.5 nM, respectively[1]. Alectinib demonstrates effective central nervous system (CNS) penetration[2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
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.
分子量
490.67
Formula
C30H26D8N4O2
CAS 号
1256585-15-5
中文名称
艾乐替尼 d8
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[3]. Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
