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1 ion step to protect three hydroxyl groups of baccatin III (1), followed by hydride ester cleavage and
2 f 500 nL of taxol (20 mM) and its precursor, baccatin III (30 mM), is separated using such a column w
3 clitaxel was prepared from 7-(triethylsilyl)-baccatin III (8) and enantioenriched N-benzoyl-2-azetidi
4                        X-ray analysis of six baccatin III analogues supports the suggested changes in
5  55 degrees C; the k' values for 10-deacetyl baccatin III and 10-deacetyl taxol go through a maximum
6     While there was no interference from the baccatin III and 10-deacetylbaccatin III, cephalomannine
7 st other naturally occurring taxanes such as baccatin III and 10-deacetylbaccatin III.
8 4-O-acetylation of 4-deacetylbaccatin III to baccatin III and 13-acetyl-4-deacetylbacatin III to 13-a
9 .4 +/- 0.5 microM and 4.9 +/- 0.3 microM for baccatin III and beta-phenylalanoyl-CoA, respectively.
10 he enantiopure side chain precursor to 7-TES-baccatin III and subsequent silyl ether deprotection aff
11     One interpretation of these data is that baccatin III and Taxol differ in their abilities to nucl
12 ural difference in microtubules formed using baccatin III and Taxol.
13  (1)H-NMR and MS verification of the product baccatin III derived from 10-deacetylbaccatin III and ac
14 cient synthesis of 13-epi-7-O-(triethylsilyl)baccatin III from 13-deoxybaccatin III is described.
15 The preparation of 13-oxo-7-O-(triethylsilyl)baccatin III from 13-epi-7-O-(triethylsilyl)baccatin III
16 h SmI(2), produced 13-epi-7-O-(triethylsilyl)baccatin III in good overall yield.
17                                    2-m-Azido baccatin III inhibited the proliferation of human cancer
18                                              Baccatin III is widely considered to be an inactive deri
19  than Taxol, we questioned whether 2-m-azido baccatin III might be active.
20 es at C4, suggesting that the C7 hydroxyl of baccatin III must remain deacylated for enzyme function.
21                                The effect of baccatin III on in vitro microtubule assembly was quanti
22 ated using the X-ray geometry of 10-deacetyl baccatin III supports the contention that the B, C, and
23                                     We found baccatin III to be active in all circumstances in which
24 mical coupling of 10-deacetylbaccatin III or baccatin III to C-13 paclitaxel side chain has been summ
25 )baccatin III from 13-epi-7-O-(triethylsilyl)baccatin III using tetrapropylammonium perruthenate and
26 ere semisynthesized from the natural product baccatin III via silyl protecting group manipulation, re
27 ontrast to 2-m-azido baccatin III, 2-p-azido baccatin III was similar to baccatin III, having no Taxo
28 Taxol, even when very high concentrations of baccatin III were employed.
29 at catalyzes the selective 13-O-acylation of baccatin III with beta-phenylalanoyl CoA as the acyl don
30     Oxidation of 13-deoxy-7-O-(triethylsilyl)baccatin III with tert-butyl peroxide, followed by reduc
31                     In contrast to 2-m-azido baccatin III, 2-p-azido baccatin III was similar to bacc
32                                              Baccatin III, an analogue of Taxol lacking the C-13 side
33 n III, 2-p-azido baccatin III was similar to baccatin III, having no Taxol-like activity, further ind
34 ibrium constants for the growth reaction for baccatin III-induced GTP-tubulin and GDP-tubulin assembl
35                                              Baccatin III-induced microtubules were routinely much lo
36 old greater than the microtubule affinity of baccatin III.
37  2'-deoxy-PTX, N-debenzoyl-2'-deoxy-PTX, and baccatin III.
38 he fact that it is essentially a substituted baccatin III.
39  measured for two forms of solid 10-deacetyl baccatin III: a dimethyl sulfoxide (DMSO) solvate and an
40 at affect this equilibrium occur between the baccatin portion of the molecule and the binding site.

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