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1 re fed diets containing 0%, 0.06%, and 0.12% exisulind.
2 d PDE-2 expression, which are the targets of exisulind.
4 we studied the effects of sulindac sulfone (exisulind), a non- cyclooxygenase-inhibitory end metabol
8 nergistic interactions for sulindac sulfide, exisulind, and NDGA with paclitaxel, cisplatin, and 13-c
10 s in cancer cells, because sulindac sulfone (exisulind, Aptosyn) and certain derivatives that inhibit
11 an colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related derivative OSI-461, b
12 hosphodiesterase inhibitor sulindac sulfone (exisulind, aptosyn, hereafter called exisulind) led to i
13 hed to an experimental diet containing 0.12% exisulind at 14 weeks after the second AOM treatment.
16 administration of the higher dose (0.12%) of exisulind during the promotion/progression stage had onl
17 s to conclude that future clinical trials of exisulind for human bladder cancer treatment and/or prev
18 studied the safety and clinical activity of exisulind in combination with capecitabine in 35 patient
20 bladder tumor cell line, HT1376, showed that exisulind inhibited growth with a GI(50) of 118 microM,
21 ulfone (exisulind, aptosyn, hereafter called exisulind) led to increased expression of the tumor supp
25 +/- retinoic acid +/- NDGA) and therapeutic (exisulind +/- paclitaxel +/- cisplatin) studies in patie
26 ies provide a rationale for chemoprevention (exisulind +/- retinoic acid +/- NDGA) and therapeutic (e
27 n to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis i
28 t treatment of human colon cancer cells with exisulind (sulindac sulfone) and related compounds induc
29 lindac sulfide, a COX-1 and COX-2 inhibitor; exisulind (sulindac sulfone), a novel proapoptotic agent
31 hemopreventive efficacy of sulindac sulfone (exisulind), the sulfone metabolite of sulindac, when adm
35 promotion/progression study and receiving 0% exisulind were switched to an experimental diet containi
36 ency (IC50 = 4-80 microM), and cisplatin and exisulind were the least potent (IC50 = 150-500 microM).
37 DE5 and PDE4 isozymes that were inhibited by exisulind with IC(50)s of 112 and 116 microM, respective
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