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1 3-infected cells are exposed only to heat or antiprogestin.
2 was controlled by topical application of an antiprogestin.
3 hysiological heat dose in the presence of an antiprogestin.
4 rst disclosure of orally active nonsteroidal antiprogestins.
5 transcription in synergy with 8-Br-cAMP and antiprogestins.
6 t time that ICI 182,780 also exhibits potent antiprogestin activity at doses frequently used in labor
7 y establish that ICI 182,780 has significant antiprogestin activity in addition to its well-documente
8 The antiestrogen tamoxifen did not display antiprogestin activity in this test system, and ICI 182,
10 e to progestins, but are growth-inhibited by antiprogestins, and underscore the need to target PR-B a
11 ould potentially be used to screen for safer antiprogestins, antiangiogenic agents, or for compounds
12 se compounds are structurally related to the antiprogestin, antiglucocorticoid, and antiandrogen drug
13 is that was blocked by co-treatment with the antiprogestin but enhanced by co-treatment with ICI.
14 ivity profiles observed with known steroidal antiprogestins, compounds of the general structural clas
15 o be effective in providing tissue-specific, antiprogestin-controllable gene expression in transgenic
17 tone (ZK98,299), were demonstrated to act as antiprogestins in vivo after oral administration to rode
18 vator that is activated by a narrow class of antiprogestins, including mifepristone and ulipristal, a
19 role in neurofibroma growth and suggest that antiprogestins may be useful in the treatment of this tu
21 hetic progestins in fish, and effects of the antiprogestin mifepristone (RU486, an abortive) are unkn
22 s a similar pharmacological profile with the antiprogestin mifepristone (RU486; Roussel Uclaf SA).
29 avior by D1-like agonists was blocked by the antiprogestin RU38486 and PR antisense oligonucleotide.
31 nvestigated the molecular basis by which the antiprogestin RU486 regulates transcription in a cell-ty
32 fulvestrant and tamoxifen, progestin R5020, antiprogestin RU486, all-trans-retinoic acid, epidermal
33 Selective receptor modulators, such as the antiprogestin RU486, are known to exhibit partial agonis
34 ain (PR1) that is activated by the synthetic antiprogestin, RU486, but not by endogenous steroid horm
36 labor suggests the presence of an endogenous antiprogestin, which we reasoned might be cortisol, whos
37 assays with the Lys-388 mutants and the pure antiprogestin ZK98299, which blocks N-/C-terminal intera
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