ライフサイエンスコーパス: TNF antagonist

1 tivity indicates that TNFR:Fc functions as a TNF antagonist.

2 autoimmune" disease effectively treated with TNF antagonists.

3 oped new-onset heart failure after receiving TNF antagonists.

4 Treatment with vedolizumab or TNF antagonists.

5 ministration-approved tumor necrosis factor (TNF) antagonists.

6 ased risk of treatment failure compared with TNF antagonists (1-year risk, 45.4% vs 34.7%; adjusted h

7 isease) vs 377 patients with incident use of TNF antagonists (206 women [54.6%]; mean [SD] age, 61.3

8 soluble TNFRIIFc (a dimorphic high-affinity TNF antagonist); (4) mice expressing TNFRIIFc transgene

9 evaluated the safety and efficacy of a novel TNF antagonist - a recombinant fusion protein that consi

10 Higher proportions of patients naive to TNF antagonists achieved endoscopic remission than patie

11 rly combined immunosuppression (ECI), with a TNF antagonist and antimetabolite might be a more effect

12 at least 6 months on combination therapy of TNF antagonists and an immunomodulator, the AGA suggests

13 failure of 1 or more tumor necrosis factor (TNF) antagonists and 44.6% had severe endoscopic disease

14 ppressants, naive to tumour necrosis factor [TNF] antagonists and vedolizumab [biologic-naive]; induc

15 fluorocitrate (a glial metabolic inhibitor), TNF antagonist, and IL-1 antagonist each blocked gp120-i

16 tion in favor of, or against, the use of non-TNF antagonist biologics in combination with an immunomo

17 ator, the AGA suggests against withdrawal of TNF antagonists, but makes no recommendation in favor of

18 p75 has been proposed to function as both a TNF antagonist by neutralizing TNF and as a TNF agonist

19 ith systemic juvenile arthritis treated with TNF antagonists display overexpression of IFN-alpha-regu

20 IL-1 and TNF antagonists each prevented gp120-induced pain change

21 potential efficacy of etanercept, a specific TNF antagonist (Enbrel).

22 Treatment starting 2 d before SNL with the TNF antagonist etanercept (1 mg, i.p., every third day)

23 Preemptive treatment with the TNF antagonist etanercept reduced SNL-induced allodynia

24 analysis involved 315 patients with previous TNF antagonist failure (ie, an inadequate response to, l

25 higher proportion of patients with previous TNF antagonist failure given vedolizumab also had a CDAI

26 Among patients who had experienced previous TNF antagonist failure, 15.2% of those given vedolizumab

27 eved endoscopic remission than patients with TNF-antagonist-failure at weeks 26 and 52.

28 Systemic administration of TNF antagonists for radiculopathy in the clinic has show

29 ted the safety and efficacy of etanercept, a TNF antagonist, for the treatment of plaque psoriasis.

30 severe Crohn's disease that was resistant to TNF antagonists had an increased rate of response to ind

31 ents with CD in whom previous treatment with TNF antagonists had failed.

32 previous therapy with tumor necrosis factor (TNF) antagonists has failed.

33 disease and consideration of a change in the TNF antagonist if the lesions are unresponsive to conven

34 s represent potential therapeutic targets of TNF antagonists in psoriasis.

35 patients treated with tumor necrosis factor (TNF) antagonists indicate that this is not a rare phenom

36 ly, low dose IKE together with etanercept, a TNF antagonist, induce ferroptosis in fibroblasts and at

37 TNF antagonist-induced psoriasis is a newly recognized a

38 Three infusions of the TNF antagonist infliximab (5 mg/kg) (n = 30) or placebo

39 Crohn disease who are naive to the chimeric TNF antagonist, infliximab.

40 imumab, a fully human tumor necrosis factor (TNF) antagonist, is an effective treatment for patients

41 gs (DMARDs), such as tumour necrosis factor (TNF) antagonists, is associated with a reduced risk of C

42 In a fraction of patients, TNF antagonists might induce new-onset heart failure or

43 g infliximab-a potent tumor necrosis factor (TNF) antagonist-on behavioral and neural measures of mot

44 nce to any TNF antagonist or vedolizumab, no TNF antagonist or vedolizumab use within 8 weeks before

45 e, loss of response to or intolerance to any TNF antagonist or vedolizumab, no TNF antagonist or vedo

46 ondary nonresponse to tumor necrosis factor (TNF) antagonists or had unacceptable side effects.

47 gher risk of treatment failure compared with TNF antagonists, particularly among patients with Crohn

48 OUND & AIMS: Although tumor necrosis factor (TNF) antagonists reduce many clinical features of inflam

49 umor necrosis factor (TNF)-alpha receptor, a TNF antagonist; septic patients were also studied.

50 g these patients with tumor necrosis factor (TNF)-antagonists significantly decreases BPH incidence.

51 een shown, and consequently various types of TNF antagonists such as etanercept and infliximab have b

52 pt and infliximab are tumor necrosis factor (TNF) antagonists that have been recently approved for th

53 Because sTNFRIIs can act as TNF antagonists, the association between recipient and d

54 e role of alternative tumor necrosis factor (TNF) antagonist therapies in the context of failure of i

55 (N = 416), which included patients naive to TNF antagonist therapy (n = 101).

56 erapies in the context of failure of initial TNF antagonist therapy in patients with rheumatoid arthr

57 the pathogenesis of rheumatoid arthritis and TNF antagonist therapy represent successes of immunology

58 After TNF antagonist therapy was discontinued and heart failur

59 After TNF antagonist therapy, 38 patients developed new-onset

60 iasis may occur any time after initiation of TNF antagonist therapy, is often of an uncommon morpholo

61 ere evaluated before and after initiation of TNF antagonist therapy.

62 I IFN activity might predict the response to TNF antagonist therapy.

63 re predictive of the therapeutic response in TNF antagonist-treated RA patients, indicating that thes

64 loss of response to, or intolerance of >/=1 TNF antagonists); we determined the proportion of patien

65 the same center who were not treated with a TNF antagonist were studied.

66 (HF) would be beneficial, clinical trials of TNF antagonists were paradoxically negative.

67 ed with at least one tumour necrosis factor (TNF) antagonist (which had failed in 96 [79%]).

68 duct, and stratified by previous exposure to TNF antagonists (yes vs no).