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l aspartic acid/sarcoma

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5 結果

Comparative distribution of free doxorubicin and poly-L-aspartic acid linked doxorubicin in MS-2 sarcoma bearing mice.

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The plasma and tissue distribution of doxorubicin-poly-L-aspartic acid (DX-PAA) and doxorubicin (DX) at equitoxic doses have been studied by a fluorescence assay in tumor bearing mice following administration of a single i.v. bolus injection. A relatively short distribution phase followed by a slow

Anti-tumor activity of daunorubicin linked to poly-L-aspartic acid.

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Daunorubicin was bound to poly-L-aspartic acid via the methylketone side chain of the drug to avoid reaction of the sugar amino group believed to be essential for optimal drug activity. Attachment of the drug to the polyamino acid by an ester linkage was achieved by nucleophylic substitution

Antitumor activity of N-(phosphonacetyl)-L-aspartic acid, a transition-state inhibitor of aspartate transcarbamylase.

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N-(Phosphonacetyl)-L-aspartate (PALA) is an analog of the transition state for the aspartate transcarbamylase reaction and has been reported previously to be a potent and specific inhibitor of de novo pyrimidine nucleotide biosynthesis. It is now shown that PALA has considerable antitumor activity

Radiation, pool size and incorporation studies in mice with 5-chloro-2'-deoxycytidine.

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Bolus doses of 5-chlorodeoxycytidine (CldC) administered with modulators of pyrimidine metabolism, followed by X-irradiation, resulted in a 2-fold dose increase effect against RIF-1 tumors in C3H mice. Pool size studies of the fate of [14C]-CldC in BDF1 mice bearing Sarcoma-180 tumors, which

Continuous five-day infusion of PALA and 5FU: a pilot phase II trial.

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In order to determine whether a simultaneous infusion of N-(phospho-n-acetyl)-L-aspartic acid (PALA) was able to increase the rate of antitumor response to 5-fluorouracil (5-FU), a pilot study was conducted. Of 10 evaluable patients with previously drug-untreated colorectal carcinoma, there were
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