1  eligibility criteria were treated with i.v. penclomedine.

2 to be on the metabolic activation pathway of penclomedine.

3  ataxia and maximum plasma concentrations of penclomedine.

4 tor aphasia were the principal toxicities of penclomedine.

5                                              Penclomedine [3,5-dichloro-4,6-dimethoxy-2-(trichloromet

6                                              Penclomedine (45 to 550 mg/ m2/d every 3 weeks) was admi

7 city was the dose-limiting toxicity (DLT) of penclomedine administered as a 1-hour infusion daily for

8 rebellar effects for 4-DM-PEN in contrast to penclomedine in a rat model, this metabolite may be a ca

9 ite may be a candidate for an alternative to penclomedine in the clinic for treatment of breast cance

10 ated to be an antitumor-active metabolite of penclomedine in vivo when evaluated against the penclome

11 of 4-DM-PEN in vitro indicates that it, like penclomedine, is also a prodrug, demonstrating a need fo

12                              Because neither penclomedine nor 4-DM-PEN were very active in vitro, the

13 tivity indicate that phase II evaluations of penclomedine on this administration schedule should be f

14  was observed to be much more cytotoxic than penclomedine or 4-DM-PEN in vitro, but evaluation of thi

15  long elimination half-life, accumulation of penclomedine over the 5 days of administration was negli

16                                 Analogues of penclomedine (PEN, 3,5-dichloro-4,6-dimethoxy-2-(trichlo

17 r brain tumors, if the cerebellar effects of penclomedine preclude its further clinical development.

18 clomedine in vivo when evaluated against the penclomedine-sensitive MX-1 human breast tumor xenograft

19 ional studies on the metabolic activation of penclomedine to identify the ultimate active form of the

20 were very active in vitro, the metabolism of penclomedine was also investigated using rat liver micro

21 olerated dose (MTD) and pharmacokinetics for penclomedine when administered as an intravenous (i.v.)