7-Ethylcamptothecin
7-Ethylcamptothecin has the superior antitumor activity than camptothecin, it has a stronger growth-inhibiting activity against tumor cells and remains in the intestinal tract for a longer time and in higher amounts when administered in vivo.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Cancer Treat Rep. 1987 Apr;71(4):341-8.
Action of 7-ethylcamptothecin on tumor cells and its disposition in mice.[Pubmed:
3829011]
Some biological effects of camptothecin (CPT) and its new derivative 7-Ethylcamptothecin (ECPT) were studied. The drugs were effective against murine leukemia; 7-Ethylcamptothecin was more effective than CPT.
METHODS AND RESULTS:
Ip administration of 7-Ethylcamptothecin or CPT gave maximum treated/control values of 325% and 232%, respectively. The drugs also inhibited the growth of KB cells in vitro, 50% effective doses of 3.5 ng/ml of 7-Ethylcamptothecin and 8.6 ng/ml of CPT, indicating the stronger activity of ECPT. Pharmacokinetic studies of the drugs in mice showed that 7-Ethylcamptothecin had a longer biological half-life in the terminal phase and a larger amount remained in the plasma compared with CPT. After iv administration of 7-Ethylcamptothecin, the drug accumulated in the intestine, suggesting that the main route of excretion of the drug is through the biliary tract. The study on cell cycle progression by flow cytometry suggested that the main effect of both drugs on L1210 cells was the blocking of G2-M phase.
CONCLUSIONS:
These results suggest that the main reasons for the superior antitumor activity of 7-Ethylcamptothecin compared with CPT are as follows: (a) 7-Ethylcamptothecin had a stronger growth-inhibiting activity against tumor cells, and (b) 7-Ethylcamptothecin remained in the intestinal tract for a longer time and in higher amounts when administered in vivo.
Biol Pharm Bull. 1995 May;18(5):648-52.
Partial purification and characterization of an esterase acting on the anticancer pro-drugs, 7-ethylcamptothecin derivatives.[Pubmed:
7492976]
METHODS AND RESULTS:
A hydrolytic enzyme which catalyzes hydrolysis of the ester-linkage of a series of 17-O-acyl derivatives of 7-Ethylcamptothecin-21-(2-dimethylamino)ethylamide [acyl derivatives of 22E] was purified from rat liver and its properties were characterized. It hydrolyzed the ester-linkage of all 22E derivatives tested as well as p-nitrophenyl acetate at pH 8-9 but had no effect on 7-ethyl-10-[4-(piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11: irinotecan), unlike CPT-11 converting carboxylesterase, which was previously purified from rat serum [Tsuji T. et al., J. Pharmacobio-Dyn., 14, 341 (1991)]. The enzyme had no effect on either acetyl choline or butyrylcholine. It was inhibited by several organophosphorous compounds such as diisopropyl fluorophosphate (DFP), bis-(p-nitrophenyl)phosphate and paraoxon, but was insensitive to inhibitors specific for choline esterases.
CONCLUSIONS:
These results indicate that this liver esterase is clearly distinct from choline esterase and serum CPT-11 converting enzyme and is able to convert pro-drugs, O-acyl derivatives of 22E, to an antitumor agent.
