ライフサイエンスコーパス: dichloroacetate

1 tions (glucose +/- palmitate +/- insulin +/- dichloroacetate).

2 rol tumors and following drug treatment with dichloroacetate.

3 vate dehydrogenase kinase-specific inhibitor dichloroacetate.

4 idosis in malaria can be treated safely with dichloroacetate.

5 c clamp, with or without coadministration of dichloroacetate.

6 l/L palmitate, and 50 microU/mL insulin plus dichloroacetate 5 mmol/L or glucose and insulin increase

7 minish this traffic in rats by administering dichloroacetate (50 mgkg) intravenously to stimulate ast

8 Dichloroacetate also decreased glucose and pyruvate prod

9 Treatment of B6.Sle1Sle2.Sle3 mice with dichloroacetate, an inhibitor of lactate production, fai

10 Exposure to dichloroacetate, an inhibitor of PDKs, increased mitocho

11 nuated in the presence of iron deficiency by dichloroacetate and imatinib, 2 putative treatments expl

12 line (when PAH is mild) and is normalized by dichloroacetate and imatinib, which both also regress me

13 pathy induced by the chemotherapeutic agents dichloroacetate and paclitaxel or HIV envelope protein g

14 Stimulation of pyruvate dehydrogenase with dichloroacetate caused a 50% decrease in plasma lactate

15 interest among the public and scientists in dichloroacetate (DCA) as a potential anticancer drug.

16 The mitochondrial kinase inhibitor dichloroacetate (DCA) has recently received attention in

17 ogical activation of PDH by cell exposure to dichloroacetate (DCA) increased production of hyperpolar

18 Dichloroacetate (DCA) is an anticancer agent that can re

19 yruvate dehydrogenase kinase inhibition with dichloroacetate (DCA) of stunned myocardium in conscious

20 e investigated the effect of the orphan drug dichloroacetate (DCA) on survival in an animal model of

21 Inhibiting PDK3 activity by dichloroacetate (DCA) or siRNA-mediated attenuation was

22 Dichloroacetate (DCA) stimulates pyruvate dehydrogenase

23 Hearts remained untreated or received dichloroacetate (DCA) to activate PDH and increase subst

24 those administered the potential neurotoxin dichloroacetate (DCA) was investigated using an intermed

25 Dichloroacetate (DCA), a compound capable of shifting me

26 us studies have found that administration of dichloroacetate (DCA), an agent that reduces lactic acid

27 However, in contrast to sodium dichloroacetate (DCA), these PDHK inhibitors did not low

28 Dichloroacetate (DCA), which is known to increase pyruva

29 uvate dehydrogenase complex (PDC) activator, dichloroacetate (DCA), would blunt activation of FOXO ge

30 inal DW-motif in inhibition of human PDK2 by dichloroacetate (DCA).

31 ific for pyruvate and its synthetic analogue dichloroacetate (DCA).

32 PDK3 was poorly inhibited by pyruvate or dichloroacetate (DCA).

33 veral commonly used antiproliferative drugs, dichloroacetate did not prevent vessel re-endothelializa

34 Activation of pyruvate dehydrogenase with dichloroacetate does not ameliorate the impairment of wh

35 Wistar rats: (1) controls, (2) rats in which dichloroacetate enhanced pyruvate dehydrogenase flux, an

36 avenous infusion with saline (CD and HFD) or dichloroacetate (HFD+DCA).

37 Dichloroacetate increased carbohydrate oxidation and the

38 Dichloroacetate increased resting pyruvate dehydrogenase

39 In vivo, dichloroacetate increased the rate of [1-(13)C]acetylcar

40 Dichloroacetate inhibits this kinase, thus enhancing PDH

41 its active site, and the pyruvate analogue, dichloroacetate, led to 16-fold more ADP than ATP being

42 vity data suggest that compounds AZD7545 and dichloroacetate lock PDK4 in the open and the closed con

43 asing glucose and insulin levels or by using dichloroacetate on the response to ischemia and reperfus

44 ) of 2.5) and to dehydrogenase activation by dichloroacetate or cAMP (twofold increase for each).

45 Monocrotaline rats were treated with oral dichloroacetate or daily imatinib injections.

46 Pharmacologic PDK2 blockade with dichloroacetate or lentiviral PDK2 knockdown prevented D

47 te, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD(+) catabolism,

48 lso aimed to identify the mechanism by which dichloroacetate overcomes this "acetyl group deficit".

49 Dichloroacetate raised baseline lCMR(glc) throughout the

50 Twenty-eight days of treatment with dichloroacetate restored PDH flux to normal levels (0.01

51 Dichloroacetate reversed the impairment of insulin-stimu

52 the pyruvate dehydrogenase kinase inhibitor dichloroacetate sharply suppressed B cell proliferation

53 inhibition of glycolytic reprogramming with dichloroacetate significantly impairs macrophage migrati

54 In vitro dichloroacetate stimulated glucose and lactate oxidation

55 pyruvate dehydrogenase complex activation by dichloroacetate, the present study examined whether ther

56 The treatment of diabetes with dichloroacetate therefore restored the balance of myocar

57 nucleophilic substitution reaction of alkyl dichloroacetates with nitroarenes react with Michael acc

58 ore whether or not increasing PDH flux, with dichloroacetate, would restore the balance of substrate