ライフサイエンスコーパス: direct-acting

1 Eradication of hepatitis C virus (HCV) using direct-acting agents (DAA) has been associated with a fi

2 d our systematic review regarding the use of direct-acting agents (DAAs) in chronic hepatitis C [2].

3 /2016-02/2017) we offered treatment with HCV direct-acting agents (DAAs) to MSM identified with a rep

4 ier to drug resistance and are the preferred direct-acting agents to achieve complete sustained virol

5 stant virus, and are some of the most potent direct-acting agents with durable sustained virologic re

6 Direct-acting agents, targeting protease and polymerase

7 rom 2002 to 2018 before and after widespread direct-acting anti-hepatitis C virus (HCV) treatment.

8 candidates are now receiving treatment with direct-acting anti-viral (DAA) agents that lower the ris

9 r-weight heparin, vitamin K antagonists, and direct-acting anticoagulants improve portal vein reperme

10 BEST PRACTICE ADVICE 12: Direct-acting anticoagulants, such as the factor Xa and

11 Direct acting antiviral (DAA) therapy is highly effectiv

12 r interferon-based dual, triple, or all-oral direct acting antiviral agent therapy, respectively, whe

13 Direct acting antiviral agents (DAA) are highly effectiv

14 alent in the renal transplant population but direct acting antiviral agents (DAA) provide an effectiv

15 Sustained virologic response (SVR) after direct acting antiviral agents (DAAs) holds promise for

16 This Perspective surveys the range of direct acting antiviral agents (DAAs) that target key st

17 ical societies presume access to an array of direct acting antiviral agents and diagnostic tests that

18 l clinical utility in combination with other direct acting antiviral agents.

19 Phase 3 trials of direct acting antiviral drugs (DAAs) for hepatitis C vir

20 It is not clear whether treatment with direct-acting antiviral (DAA) agents affects risk of CVD

21 response 12 weeks after therapy (SVR12) with direct-acting antiviral (DAA) agents for recurrent HCV i

22 once patients began receiving treatment with direct-acting antiviral (DAA) agents, from 2014 through

23 lving from interferon (IFN)-based therapy to direct-acting antiviral (DAA) agents, yet some safety co

24 fe efficacy and tolerance data with all-oral direct-acting antiviral (DAA) combinations in these pati

25 has been suggested to be less responsive to direct-acting antiviral (DAA) drug treatment than other

26 esponse (SVR) have not been evaluated in the direct-acting antiviral (DAA) era.

27 the reach and capacity of the VA to deliver direct-acting antiviral (DAA) HCV therapy, supported by

28 trials in subjects previously treated with a direct-acting antiviral (DAA) regimen.

29 Highly effective direct-acting antiviral (DAA) regimens (90% efficacy) ar

30 New direct-acting antiviral (DAA) regimens are available.

31 Direct-acting antiviral (DAA) regimens are safe and effe

32 py have led to the approval of multiple oral direct-acting antiviral (DAA) regimens by the U.S. Food

33 Direct-acting antiviral (DAA) regimens without IFN are n

34 is C virus (HCV) consists of interferon-free direct-acting antiviral (DAA) regimens, including combin

35 infected chimpanzees during treatment with a direct-acting antiviral (DAA) targeting the HCV NS5b pol

36 BACKGROUND & AIMS: Interferon-free direct-acting antiviral (DAA) therapies are effective in

37 Direct-acting antiviral (DAA) therapies are effective in

38 Although direct-acting antiviral (DAA) therapies for chronic hepa

39 There is controversy over the effects of direct-acting antiviral (DAA) therapies for hepatitis C

40 sponse (SVR) at 12 weeks after completion of direct-acting antiviral (DAA) therapy (SVR(12) ).

41 evidence describing the interaction between direct-acting antiviral (DAA) therapy for hepatitis and

42 Direct-acting antiviral (DAA) therapy for hepatitis C vi

43 Direct-acting antiviral (DAA) therapy for hepatitis C vi

44 ere is controversy regarding the benefits of direct-acting antiviral (DAA) therapy for hepatitis C vi

45 e in Australia, given unrestricted access to direct-acting antiviral (DAA) therapy from 2016.

46 e in Australia, given unrestricted access to direct-acting antiviral (DAA) therapy from 2016.

47 Direct-acting antiviral (DAA) therapy has altered the fr

48 The success of direct-acting antiviral (DAA) therapy has led to near-un

49 Direct-acting antiviral (DAA) therapy has transformed th

50 The efficacy and safety of all-oral direct-acting antiviral (DAA) therapy in HCV-associated

51 Direct-acting antiviral (DAA) therapy is highly effectiv

52 Direct-acting antiviral (DAA) therapy, recently approved

53 pid changes in metabolic parameters early in direct-acting antiviral (DAA) therapy.

54 titis C virus-infected individuals receiving direct-acting antiviral (DAA) therapy.

55 daily to twice-daily hepatitis C virus (HCV) direct-acting antiviral (DAA) therapy.

56 results as proxy measures for initiation of direct-acting antiviral (DAA) treatment and sustained vi

57 Recent introduction of all-oral direct-acting antiviral (DAA) treatment has revolutioniz

58 ed the cost-effectiveness of two alternative direct-acting antiviral (DAA) treatment policies in a re

59 of HCV staging, specialist teleconsultation, direct-acting antiviral (DAA) treatment, and sustained v

60 While direct-acting antiviral (DAA) treatments are effective,

61 mission in the context of different rates of direct-acting antiviral (DAA) use.

62 erably with the approval of interferon-free, direct-acting antiviral (DAA)-based combination therapie

63 (HCV) genotype 1-infected patients who fail direct-acting antiviral (DAA)-based regimens remains unk

64 ve sustained virological response (SVR) with direct-acting antiviral (DAA).

65 10), protease inhibitor (PI; 2011-2013), and direct-acting antiviral (DAA; 2014-2015).

66 s Health Administration (29,033 treated with direct-acting antiviral [DAA] agents and 19,102 treated

67 Voxilaprevir is a direct-acting antiviral agent (DAA) that targets the NS3

68 risk of hepatocellular carcinoma (HCC) after direct-acting antiviral agent (DAA) treatment.

69 BACKGROUND & AIMS: Daclatasvir is a direct-acting antiviral agent and potent inhibitor of NS

70 Daclatasvir is a direct-acting antiviral agent and potent inhibitor of NS

71 support further evaluation of the three-drug direct-acting antiviral agent regimen of grazoprevir 100

72 Remdesivir (RDV) is a direct-acting antiviral agent that is used to treat pati

73 Resumption of direct-acting antiviral agent therapy after a temporary

74 n who had not been treated previously with a direct-acting antiviral agent were assigned randomly to

75 The combination of three direct-acting antiviral agents (AL-335, odalasvir, and s

76 potential drug-drug interactions between HCV direct-acting antiviral agents (DAA) and HIV antiretrovi

77 New direct-acting antiviral agents (DAA) offer an unpreceden

78 Direct-acting antiviral agents (DAAs) are highly effecti

79 Direct-acting antiviral agents (DAAs) are used increasin

80 R) is a validated surrogate outcome and that direct-acting antiviral agents (DAAs) have been demonstr

81 nse after treatment with regimens containing direct-acting antiviral agents (DAAs) have limited retre

82 actions between antiretroviral drugs and HCV direct-acting antiviral agents (DAAs) must be carefully

83 Direct-acting antiviral agents (DAAs) represent the stan

84 Developments in directed use of new direct-acting antiviral agents (DAAs) to eliminate circu

85 Several new HCV therapies, called direct-acting antiviral agents (DAAs), are available tha

86 V infection could be cured by treatment with direct-acting antiviral agents alone in the absence of i

87 atment landscape and addition of several new direct-acting antiviral agents and combination regimens

88 very of antiviral immunity, a combination of direct-acting antiviral agents and immunotherapy are lik

89 Current therapies with all-oral direct-acting antiviral agents are associated with high

90 Direct-acting antiviral agents are highly efficient trea

91 Survival data with direct-acting antiviral agents are not available.

92 To shorten the course of direct-acting antiviral agents for chronic hepatitis C v

93 ration has recently approved a number of new direct-acting antiviral agents for the treatment of chro

94 Direct-acting antiviral agents have not been studied exc

95 Second generation direct-acting antiviral agents have revolutionized thera

96 azoprevir (an NS3/4A protease inhibitor) are direct-acting antiviral agents recently approved in the

97 azoprevir (an NS3/4A protease inhibitor) are direct-acting antiviral agents recently approved in the

98 The development of direct-acting antiviral agents that can cure a chronic h

99 The advent of direct-acting antiviral agents to treat hepatitis C viru

100 l Hepa-C registry who started treatment with direct-acting antiviral agents while awaiting LT were id

101 le data regarding drug-drug interactions for direct-acting antiviral agents, the interactions being t

102 With the advent of direct-acting antiviral agents, there has been a rapid r

103 re are currently no approved treatments with direct-acting antiviral agents.

104 3 who had failed an all-oral regimen of >/=2 direct-acting antiviral agents.

105 had failed an all-oral regimen of 2 or more direct-acting antiviral agents.

106 We review recent advances in development of direct-acting antiviral and host-targeting agents, some

107 Early HCV treatment with all-oral direct-acting antiviral combination therapy has been ass

108 een developed as a part of a three-component direct-acting antiviral combination therapy.

109 For direct-acting antiviral combinations only weak associati

110 All-oral direct-acting antiviral drugs (DAAs) for hepatitis C vir

111 ization outlines the use of highly effective direct-acting antiviral drugs (DAAs) to achieve eliminat

112 New direct-acting antiviral drugs for the treatment of chron

113 ase is a prime target for the development of direct-acting antiviral drugs for the treatment of chron

114 Direct-acting antiviral drugs have a high cure rate and

115 w studies have reported the effectiveness of direct-acting antiviral drugs in these patients.

116 assessed the efficacy and safety of the two direct-acting antiviral drugs ombitasvir, an NS5A inhibi

117 e to short-course combination therapies with direct-acting antiviral drugs that might be explored in

118 gy, which has led to development of many new direct-acting antiviral drugs that target key components

119 In the modern direct-acting antiviral era, calculated likely KDPI over

120 st HCV reinfection in MSM was similar in the direct-acting antiviral era, compared to the interferon

121 In the pre-direct-acting antiviral era, they accounted for 7.2%, 26

122 e taken place over time, particularly in the direct-acting antiviral era.

123 terferon and ribavirin (PegIFN-RBV) plus one direct-acting antiviral in 53.4%, PegIFN-RBV in 34.5%, a

124 transient suppression of RHV viremia with a direct-acting antiviral led to the priming of CD8 T cell

125 er the elimination of hepatitis C virus with direct-acting antiviral normalizes expression of IFN-sti

126 irst large-scale prospective study reporting direct-acting antiviral outcomes in sub-Saharan Africa.

127 The pangenotypic direct-acting antiviral regimen of glecaprevir coformula

128 e treatment) can affect the efficacy of this direct-acting antiviral regimen, and pretreatment resist

129 he once-daily, ribavirin-free, pangenotypic, direct-acting antiviral regimen, glecaprevir coformulate

130 Sofosbuvir-velpatasvir, a pangenotypic direct-acting antiviral regimen, was preemptively admini

131 clinical care treatment cohort, treated with direct-acting antiviral regimens between January 1, 2014

132 an ultrarapid virological response on triple direct-acting antiviral regimens by day 2 and received 3

133 No all-oral, direct-acting antiviral regimens have been approved for

134 disease, highly efficacious, well-tolerated, direct-acting antiviral regimens have not been extensive

135 Short-course, oral, curative, direct-acting antiviral regimens have transformed treatm

136 ween race/ethnicity and effectiveness of new direct-acting antiviral regimens in the Veterans Affairs

137 nsideration of the use of newer pangenotypic direct-acting antiviral regimens in this region.

138 iviral activity of all-oral, ribavirin-free, direct-acting antiviral regimens requires evaluation in

139 In addition, there are now direct-acting antiviral regimens specifically approved f

140 ogression and are less responsive to current direct-acting antiviral regimens than patients infected

141 irologic response after prior treatment with direct-acting antiviral regimens that included the nucle

142 With the development of direct-acting antiviral regimens that offer high sustain

143 etermine whether more potent interferon-free direct-acting antiviral regimens will allow treatment du

144 Data outside of clinical trials with direct-acting antiviral regimens with or without ribavir

145 The transmission of direct-acting antiviral resistance-associated substituti

146 With no available direct-acting antiviral targeting DENV, NS2/NS3 protease

147 Though highly effective direct-acting antiviral therapies are costly, the price

148 With newer, direct-acting antiviral therapies for HCV, our objective

149 We review the status of direct-acting antiviral therapies for hepatitis C virus

150 Currently available direct-acting antiviral therapies have reduced efficacy

151 e for larger studies of shortened courses of direct-acting antiviral therapies in persons with HIV in

152 Highly effective hepatitis C virus (HCV) direct-acting antiviral therapies that do not require mo

153 nd NS5A are clinically validated targets for direct-acting antiviral therapies.

154 ny of whom cannot attain the new, expensive, direct-acting antiviral therapies.

155 ers of both humanized mice and patients, and direct-acting antiviral therapy attenuated M2 macrophage

156 r pre-emptive administration of pangenotypic direct-acting antiviral therapy can safely prevent the d

157 the advent of highly effective and tolerable direct-acting antiviral therapy has paved the way for HC

158 e point-of-care diagnostics and pangenotypic direct-acting antiviral therapy is essential to achieve

159 Scale-up of direct-acting antiviral therapy is expected to abate hep

160 nfections are identified and the response to direct-acting antiviral therapy is monitored.

161 Direct-acting antiviral therapy is now curative, but it

162 Combination direct-acting antiviral therapy of 8-24 weeks is highly

163 arge prospective observational cohort study, direct-acting antiviral therapy with SOF/ledipasvir, omb

164 the efficacy and safety of sofosbuvir-based direct-acting antiviral therapy, individually tailored a

165 changed by the advent of safe and effective direct-acting antiviral therapy, such that most patients

166 ls increased within 2 weeks after initiating direct-acting antiviral therapy.

167 tion drug use remains a barrier to accessing direct-acting antiviral treatment (DAA) for hepatitis C

168 Direct-acting antiviral treatment for hepatitis C virus

169 Conclusion: Those achieving SVR after direct-acting antiviral treatment had significantly lowe

170 ective salvage therapy for patients for whom direct-acting antiviral treatment has failed.

171 n) was an implementation trial providing HCV direct-acting antiviral treatment in Melbourne, Australi

172 virologic response (SVR) on mortality after direct-acting antiviral treatment is not well documented

173 In clinical trials of interferon-free, direct-acting antiviral treatment of chronic hepatitis C

174 Scaling up direct-acting antiviral treatment, syringe service progr

175 report the prevalence of RASs in a cohort of direct-acting antiviral treatment-naive, gt3-infected pa

176 rojected the effect of the administration of direct-acting antiviral treatments until Feb 28, 2019, a

177 response (SVR) with hepatitis C virus (HCV) direct-acting antiviral-based regimens is commonly assoc

178 ience virologic failure after treatment with direct-acting antiviral-based therapies remains unclear.

179 etreatment of patients who previously failed direct-acting antiviral-based therapies with sofosbuvir-

180 r, daclatasvir, simeprevir, and ribavirin in direct-acting antiviral-experienced patients, as recomme

181 This study evaluated the impact of direct-acting antiviral-induced SVR on all-cause mortali

182 Direct-acting antiviral-mediated clearance of HCV is ass

183 re, Civacir is equally active against tested direct-acting antiviral-resistant HCV isolates in cell c

184 ralization of different HCV genotypes and of direct-acting antiviral-resistant viruses.

185 ses and define this nucleotide analogue as a direct-acting antiviral.

186 ded into interferon, protease inhibitor, and direct-acting antiviral.

187 pharmacokinetics (PK) of the ribavirin-free, direct-acting, antiviral, fixed-dose combination of glec

188 s the efficacy and safety of a once-daily, 2-direct-acting-antiviral-agent (2-DAA) combination of sim

189 h sofosbuvir (SOF) in combination with other direct acting antivirals (DAAs) and the antiarrhythmic d

190 Despite the development of potent direct acting antivirals (DAAs) for HCV treatment, a vac

191 All-oral direct acting antivirals (DAAs) have been shown to have

192 High costs of direct acting antivirals (DAAs) led healthcare insurers

193 can be restored after viral eradication with direct acting antivirals (DAAs).

194 Including the effects of direct acting antivirals in our models, we found that in

195 Direct-acting antivirals (DAA) for hepatitis C virus (HC

196 With the increasing use of direct-acting antivirals (DAA) for treatment of chronic

197 The effectiveness of interferon-free direct-acting antivirals (DAA) in treating chronic hepat

198 er sustained virological response (SVR) with direct-acting antivirals (DAA) is unclear.

199 There is a lack of data on the use of direct-acting antivirals (DAA) on the risk of death and

200 nt for hepatitis C virus (HCV) with all-oral direct-acting antivirals (DAA) therapy is now entering i

201 itis C (CHC) patients after eradication with direct-acting antivirals (DAA) would increase 25-hydroxy

202 patients with advanced fibrosis treated with direct-acting antivirals (DAA).

203 ed hepatitis C virus (HCV) patients involves direct-acting antivirals (DAA).

204 HIV/HCV with advanced fibrosis treated with direct-acting antivirals (DAA).

205 HCV virologic response after treatment with direct-acting antivirals (DAA).

206 Direct-acting antivirals (DAAs) against hepatitis C viru

207 Direct-acting antivirals (DAAs) against Hepatitis C viru

208 whether HCV-elimination by sofosbuvir-based direct-acting antivirals (DAAs) and addition of RBV impr

209 n to re-treat patients who do not respond to direct-acting antivirals (DAAs) and the feasibility of f

210 Direct-acting antivirals (DAAs) are becoming accessible

211 Direct-acting antivirals (DAAs) effectively eradicate ch

212 ronic hepatitis C virus (HCV) infection with direct-acting antivirals (DAAs) for 6 weeks achieves sus

213 The cost of direct-acting antivirals (DAAs) for hepatitis C virus (H

214 s (HCV) treatment through the development of direct-acting antivirals (DAAs) has generated internatio

215 Recent approval of HCV direct-acting antivirals (DAAs) has renewed discussions

216 The advent of direct-acting antivirals (DAAs) has transformed the land

217 es has evolved rapidly as safe and effective direct-acting antivirals (DAAs) have become the standard

218 Direct-acting antivirals (DAAs) have changed the landsca

219 High costs of direct-acting antivirals (DAAs) have led health-care ins

220 Direct-acting antivirals (DAAs) have led to a high cure

221 The availability of safe, efficacious, oral direct-acting antivirals (DAAs) have ushered in a new er

222 reatment guidelines that advocate the use of direct-acting antivirals (DAAs) in all patients.

223 he immune effects of viral load decline with direct-acting antivirals (DAAs) in blood.

224 Data on IFN-free regimens combining direct-acting antivirals (DAAs) in HCV-associated lympho

225 Treatment for hepatitis C virus (HCV) with direct-acting antivirals (DAAs) in hepatitis B virus (HB

226 real-world data on the effectiveness of oral direct-acting antivirals (DAAs) in predominantly minorit

227 the major advances since the introduction of direct-acting antivirals (DAAs) in the management of HCV

228 Often, availability of all-oral direct-acting antivirals (DAAs) is delayed because of di

229 r impact in patients with cirrhosis cured by direct-acting antivirals (DAAs) is still undefined.

230 hortening the duration of treatment with HCV direct-acting antivirals (DAAs) leads to substantial cos

231 Oral direct-acting antivirals (DAAs) represent a major advanc

232 Direct-acting antivirals (DAAs) show excellent results i

233 Direct-acting antivirals (DAAs) targeting hepatitis C vi

234 strains, there is a pressing need to develop direct-acting antivirals (DAAs) to combat such deadly vi

235 ate resistance of hepatitis C virus (HCV) to direct-acting antivirals (DAAs), due to the small number

236 rgets, it is essential to increase access to direct-acting antivirals (DAAs), especially among people

237 In the era of direct-acting antivirals (DAAs), it is unclear whether t

238 In the era of highly effective direct-acting antivirals (DAAs), many questions pertaini

239 d on interferon-alpha, ribavirin and the new direct-acting antivirals (DAAs), such as NS3 protease an

240 With the approval of direct-acting antivirals (DAAs), the management of drug-

241 has led to the discovery of new HCV-specific direct-acting antivirals (DAAs), which have an unprecede

242 tients with sustained virologic responses to direct-acting antivirals (DAAs), which lack immunomodula

243 HIV-infected MSM) in Germany rose before HCV direct-acting antivirals (DAAs).

244 patitis C virus (HCV) infection treated with direct-acting antivirals (DAAs).

245 viduals, and the potential for resistance to direct-acting antivirals (DAAs).

246 its trajectory with or without scaled-up HCV direct-acting antivirals (DAAs).

247 m, JAILFREE-C, to treat HCV in prisons using direct-acting antivirals (DAAs).

248 rapies (8-24 weeks) or interferon (IFN)-free direct-acting antivirals (DAAs; 8-12 weeks, 95% sustaine

249 em and preventing recurrent hepatitis C with direct-acting antivirals (DDAs) may only have a limited

250 T integrated data from recent trials of oral direct-acting antivirals (SOLAR 1 and 2), the United Net

251 Recent development of direct-acting antivirals against HCV including NS3/4A pr

252 Highly effective direct-acting antivirals against Hepatitis C virus (HCV)

253 espite the recent success of newly developed direct-acting antivirals against hepatitis C, the diseas

254 Hepatitis C virus (HCV) direct-acting antivirals are highly effective.

255 Treatment with direct-acting antivirals for HCV and wider use of tenofo

256 re-LT versus post-LT HCV treatment with oral direct-acting antivirals for patients with MELD scores b

257 l and subtropical regions, with no available direct-acting antivirals for treatment.

258 The availability of oral direct-acting antivirals has altered the hepatitis C vir

259 atitis C virus (HCV) treatment regimens with direct-acting antivirals have not been extensively studi

260 the prevalence of RAVs to currently approved direct-acting antivirals in a large European population

261 Studies using direct-acting antivirals in patients with CKD and those

262 The development of direct-acting antivirals in recent years has dramaticall

263 Limited data are available on direct-acting antivirals in the transplant setting for p

264 es, and evaluate the effect of these RASs on direct-acting antivirals in vitro.

265 ment as prevention with highly effective new direct-acting antivirals is a prospective HCV eliminatio

266 rferon-free, guideline-tailored therapy with direct-acting antivirals is highly effective and safe fo

267 Modern direct-acting antivirals may modify this risk.

268 ted with HCV transmission and treatment with direct-acting antivirals may prevent further HCV infecti

269 Direct-acting antivirals produce high SVR rates in white

270 th increased treatment uptake and the use of direct-acting antivirals reduced incidence by 77% (from

271 opment of multiple highly effective and safe direct-acting antivirals to treat hepatitis C virus (HCV

272 brosis assessments) were obtained onsite and direct-acting antivirals were coadministered with methad

273 sed, 45 334 (30.2%) initiated treatment with direct-acting antivirals, and 29 090 (19.4%) achieved a

274 We assessed the combination of two direct-acting antivirals, ombitasvir (NS5A inhibitor) an

275 era of nearly 100% HCV cure rates thanks to direct-acting antivirals, these findings encourage the m

276 provements coincide with the availability of direct-acting antivirals, which resulted in a 100% SVR r

277 ls, enabled the discovery and development of direct-acting antivirals.

278 orted with this approach in combination with direct-acting antivirals.

279 tion of resistant viruses than treating with direct-acting antivirals.

280 serve as an attractive target in developing direct-acting antivirals.

281 s global disease despite the availability of direct-acting antivirals.

282 uded increase in treatment uptake and use of direct-acting antivirals.

283 of interferon-free, all-oral combinations of direct-acting antivirals.

284 ologic responses (SVRs) after treatment with direct-acting antivirals.

285 ly infected with HCV undergoing therapy with direct-acting antivirals.

286 nced virologic failure in clinical trials of direct-acting antivirals.

287 nalyzed for the presence of RASs to approved direct-acting antivirals.

288 ed more often in patients on warfarin versus direct acting oral anticoagulant (16.7% versus10.0%).

289 Patients on warfarin versus direct acting oral anticoagulant were equally likely to

290 20.2% received warfarin while 79.8% received direct acting oral anticoagulant.

291 ng is not indicated among patients receiving direct-acting oral anticoagulant therapy.

292 Those who used regular aspirin, warfarin, or direct-acting oral anticoagulants (DOACs) were defined a

293 , argatroban, bivalirudin, or one of the new direct-acting oral anticoagulants as appropriate.

294 Apixaban and rivaroxaban, both direct-acting oral anticoagulants, are being increasingl

295 cific guidance for vitamin K antagonists and direct-acting oral anticoagulants; 4) evaluate whether t

296 Ticagrelor is a direct-acting P2Y12 inhibitor and, unlike clopidogrel an

297 l counterscreens identified a first-in-class direct-acting RABV inhibitor, GRP-60367, with a specific

298 These reports of direct-acting RAS inhibitors provide valuable insight fo

299 In this article, the discovery of selective, direct acting S1P1 agonists utilizing an ethanolamine sc

300 ng scientific concepts, with 135 projects on direct-acting small molecules that represent new classes