Size: | Price | Quantity | |
---|---|---|---|
10 mg | $70.00 | ||
50 mg | $240.00 |
Pemetrexed (357166-29-1) is a multi-targeted antifolate with antitumor activity. It potently inhibits folate-dependent enzymes involved in both purine and pyrimidine synthesis including thymidylate synthase (Ki = 109 nM), dihydrofolate reductase (Ki = 7 nM), glycinamide ribonucleotide formyltransferase (Ki = 9.3 μM), and aminoimidazole carboxamide ribonucleotide formyltransferase (Ki = 3.6 μM).1 A clinically useful anticancer agent.2 Indirectly activates the metabolic kinase AMPK and consequently influences the mTORC1 pathway in human carcinomas.3 Activation of AMPK is associated with pemetrexed resistance.4 Induces G0/G1-phase cell cycle arrest in esophageal squamous cell carcinoma cells.5
References/Citations:
1) Shih et al. (1997), LY231514, a pyrrolo[2,3-d]pyrimidine-based antifolate that inhibits multiple folate-requiring enzymes; Cancer Res. 57 1116
2) Hanauske et al. (2001), Pemetrexed disodium: a novel antifolate clinically active against multiple solid tumors; Oncologist 6 363
3) Rothbart et al. (2010), Pemetrexed indirectly activates the metabolic kinase AMPK in human carcinomas; Cancer Res. 70 10299
4) Qin et al. (2019), AMPK activation induced in pemetrexed-treated cells is associated with development of drug resistance independently of target enzyme expression; Mol. Oncol. 13 1419
5) Li et al. (2019), Pemetrexed exerts anticancer effects by inducing G0/G1-phase cell cycle arrest and activating the NOXA/Mcl-1 axis in human esophageal squamous cell carcinoma cells; Oncol. Lett. 17 1851
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Pemetrexed (357166-29-1) is a multi-targeted antifolate with antitumor activity. It potently inhibits folate-dependent enzymes involved in both purine and pyrimidine synthesis including thymidylate synthase (Ki = 109 nM), dihydrofolate reductase (Ki = 7 nM), glycinamide ribonucleotide formyltransferase (Ki = 9.3 μM), and aminoimidazole carboxamide ribonucleotide formyltransferase (Ki = 3.6 μM).1 A clinically useful anticancer agent.2 Indirectly activates the metabolic kinase AMPK and consequently influences the mTORC1 pathway in human carcinomas.3 Activation of AMPK is associated with pemetrexed resistance.4 Induces G0/G1-phase cell cycle arrest in esophageal squamous cell carcinoma cells.5
References/Citations:
1) Shih et al. (1997), LY231514, a pyrrolo[2,3-d]pyrimidine-based antifolate that inhibits multiple folate-requiring enzymes; Cancer Res. 57 1116
2) Hanauske et al. (2001), Pemetrexed disodium: a novel antifolate clinically active against multiple solid tumors; Oncologist 6 363
3) Rothbart et al. (2010), Pemetrexed indirectly activates the metabolic kinase AMPK in human carcinomas; Cancer Res. 70 10299
4) Qin et al. (2019), AMPK activation induced in pemetrexed-treated cells is associated with development of drug resistance independently of target enzyme expression; Mol. Oncol. 13 1419
5) Li et al. (2019), Pemetrexed exerts anticancer effects by inducing G0/G1-phase cell cycle arrest and activating the NOXA/Mcl-1 axis in human esophageal squamous cell carcinoma cells; Oncol. Lett. 17 1851
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