ライフサイエンスコーパス: cytotoxic agent

1 tibody conjugated to calicheamicin, a potent cytotoxic agent.

2 tibody conjugated to calicheamicin, a potent cytotoxic agent.

3 little activity as either an antitubulin or cytotoxic agent.

4 h inhibited when bexarotene was added to the cytotoxic agent.

5 by invading cancerous cells and releasing a cytotoxic agent.

6 oxide (UHP) is a stable form of H(2)O(2) and cytotoxic agent.

7 erapeutic potential as a tumor cell-specific cytotoxic agent.

8 n chromophore, was also found to be a potent cytotoxic agent.

9 is both glycoengineered and conjugated to a cytotoxic agent.

10 s biomarker was harnessed to uncage a potent cytotoxic agent.

11 antigen with the delivery of a highly potent cytotoxic agent.

12 on, with iron and reactive oxygen species as cytotoxic agents.

13 ytostatic influence of the CDK-inhibitor and cytotoxic agents.

14 s aimed at improving the efficacy of current cytotoxic agents.

15 sed for the targeted delivery and release of cytotoxic agents.

16 treatment with combinations of conventional cytotoxic agents.

17 ndrial priming might enhance the efficacy of cytotoxic agents.

18 gimen designed to decrease exposure to other cytotoxic agents.

19 xpression of enzymes, which are inhibited by cytotoxic agents.

20 een implicated in resistance to TRAIL and to cytotoxic agents.

21 t from the literature for several well-known cytotoxic agents.

22 tions of targeted therapies with traditional cytotoxic agents.

23 vation induced by growth factors and by some cytotoxic agents.

24 fer from those associated with cytokines and cytotoxic agents.

25 yeloma cell lines, enhancing the activity of cytotoxic agents.

26 her as a single agent or in combination with cytotoxic agents.

27 mitations associated with currently employed cytotoxic agents.

28 be involved in the resistance of BL cells to cytotoxic agents.

29 ciated with increased resistance of cells to cytotoxic agents.

30 duce, not immunogenic, and easily coupled to cytotoxic agents.

31 ial for in vivo delivery of radioisotopes or cytotoxic agents.

32 atin and etoposide continue to be the chosen cytotoxic agents.

33 oids alone and a combination of steroids and cytotoxic agents.

34 provide a way to reduce systemic exposure to cytotoxic agents.

35 entarium has led to multiple combinations of cytotoxic agents.

36 f which are different from those of standard cytotoxic agents.

37 the N-methylsansalvamide peptides are potent cytotoxic agents.

38 hologic tissue damage through the release of cytotoxic agents.

39 nfirms that these VEGFR-2 inhibitors are not cytotoxic agents.

40 utathione biosynthesis, is regulated by many cytotoxic agents.

41 he antiproliferative effects of conventional cytotoxic agents.

42 ng groups for intracellular cleavage of free cytotoxic agents.

43 activity of FTIs and their interactions with cytotoxic agents.

44 kely be in combination with more established cytotoxic agents.

45 s of growth factor deprivation or to various cytotoxic agents.

46 portant part of the defense of cells against cytotoxic agents.

47 se rapidly in hepatocytes exposed to broadly cytotoxic agents.

48 t affect the sensitivity of this organism to cytotoxic agents.

49 heir sensitivity to several non-DNA-damaging cytotoxic agents.

50 ed in the response of hematopoietic cells to cytotoxic agents.

51 uman T98G glioblastoma cells to a variety of cytotoxic agents.

52 to ameliorate resistance of tumours against cytotoxic agents.

53 renders colon cancer cells more resistant to cytotoxic agents.

54 ates are monoclonal antibodies conjugated to cytotoxic agents.

55 nd conjugation of the monoclonal antibody to cytotoxic agents.

56 rogated by the presence of leukemia cells or cytotoxic agents.

57 ce to structurally different antibiotics and cytotoxic agents.

58 r development despite wielding an arsenal of cytotoxic agents.

59 -renewal, differentiation, and resistance to cytotoxic agents.

60 ity of OVCAR8/ADR cells to Pgp-transportable cytotoxic agents.

61 r immune biomarkers of clinical responses to cytotoxic agents.

62 n combined with standard chemotherapeutic or cytotoxic agents.

63 elopment that could be applied to many other cytotoxic agents.

64 atural products that produce them are potent cytotoxic agents.

65 m for SRC-3 and TRAF4-mediated resistance to cytotoxic agents.

66 (4a-g) as potential minor groove binders and cytotoxic agents.

67 blocked these events in cells exposed to the cytotoxic agent 1-beta-d-arabinofuranosylcytosine (ara-C

68 own previously that the target of the potent cytotoxic agent 4-[(7-bromo-2-methyl-4-oxo-3H-quinazolin

69 rformed structural studies and show that the cytotoxic agent 7A-O-demethoxy-amino-noscapine (7A-amino

70 role of p130(Cas) (Cas) in resistance to the cytotoxic agent Adriamycin.

71 Demonstration of long-lived cytotoxic agents after Pseudomonas infection may establi

72 l synthesis of demethyl calamenene, a potent cytotoxic agent against human adenocarcinoma A 549.

73 new compounds, BIHC was found to be the most cytotoxic agent against the HepG2 cell line while exhibi

74 (thiazol-5-yl)pyrimidin-2-amines were potent cytotoxic agents against cancer cell lines, suppressed m

75 e PARP-1 inhibitors to enhance the effect of cytotoxic agents against cancer cell lines.

76 found to be superior to the combination of a cytotoxic agent and corticosteroids.

77 ia in human cancers compared to the parental cytotoxic agent and the vehicle groups.

78 ising strategy for the selective delivery of cytotoxic agents and fluorescent markers to hypoxic tiss

79 and nanomaterials have been investigated as cytotoxic agents and inhibitors, in photodynamic therapy

80 n cancer focus on novel drug combinations of cytotoxic agents and molecular targeted agents or novel

81 ovarian cancer based on drug combinations of cytotoxic agents and molecular targeted agents, delivere

82 Cancer chemotherapy has evolved from cytotoxic agents and now includes several new agents tha

83 y observed in patients with GPA treated with cytotoxic agents and should be avoided in these patients

84 ion of these agents differ from conventional cytotoxic agents and surrogate markers for inhibition of

85 n 30 months with the integration of multiple cytotoxic agents and targeted therapies.

86 ase to the use of varied hormonal analogues, cytotoxic agents and targeted therapy for the management

87 Antitumor activity of cytotoxic agents and the epidermal growth factor recepto

88 lta), or both (dph3Delta) for sensitivity to cytotoxic agents and thermal stress.

89 ly are differentially susceptible to various cytotoxic agents and treatments.

90 The tumor target, the cytotoxic agent, and the manner in which the agent is at

91 Corticosteroids, novel agents, conventional cytotoxic agents, and high-dose chemotherapy with autotr

92 tiate cancer immunotherapy from conventional cytotoxic agents, and we discuss their implications for

93 air could affect the sensitivity of cells to cytotoxic agents, and would therefore be an important co

94 l death induced by only a selected subset of cytotoxic agents (antimicrotubule agents and a topoisome

95 ne-refractory prostate cancer, including new cytotoxic agents, antiproliferative agents, immune-based

96 The antibody and the cytotoxic agent are conjugated by means of a stable link

97 have been identified and the means by which cytotoxic agents are appended to antibodies has been gre

98 While potent cytotoxic agents are available to oncologists, the clini

99 Alternatives to cytotoxic agents are desirable for patients with HIV-ass

100 sts that the use of efaproxiral instead of a cytotoxic agent, as a radiation sensitizer, may be advan

101 w platinum compounds, new taxanes, and other cytotoxic agents, as well as non-cytotoxic compounds wit

102 produce high localized concentrations of the cytotoxic agent at the tumor site while limiting systemi

103 loss of ovarian function due to exposure to cytotoxic agents, but GnRHa use for ovarian protection i

104 rs do not protect cancer cells from death by cytotoxic agents, but may switch drug-induced apoptosis

105 Hence, BAPOs may be suitable as photolatent cytotoxic agents, but such applications have not been in

106 ed lavendustin A analogues, may be acting as cytotoxic agents by a mechanism involving the inhibition

107 16, HCT-116/VM46, resistant to many standard cytotoxic agents by means of a multiple drug resistance

108 trate that HDAC10 protects cancer cells from cytotoxic agents by mediating autophagy and identify thi

109 ans of a monoclonal antibody conjugated to a cytotoxic agent, calicheamicin.

110 cancers and consider how the use of existing cytotoxic agents can be optimised for this patient group

111 With this protocol, analogues of the cytotoxic agent chamaecypanone C have been synthesized v

112 t associated with general sensitivity to the cytotoxic agents cis-platin, placitaxel, and gemcitabine

113 ere examined in vivo after exposure to three cytotoxic agents (Cisplatin, Nitrogen Mustard and N-meth

114 molecular chaperone, induced by low doses of cytotoxic agents, clears cell debris.

115 In the presence of cytotoxic agents, colonies reduced their variance in gro

116 Cisplatin is a potent cytotoxic agent commonly used for the treatment of solid

117 showed profound chemoresistance to multiple cytotoxic agents compared with adherent cultures, which

118 erapies enhancing cancer cell sensitivity to cytotoxic agents could significantly improve patient out

119 Drug conjugates are chemotherapeutic or cytotoxic agents covalently linked to targeting ligands

120 Distinct cytotoxic agents currently used in the oncological armam

121 b-PCL) micelles were loaded with paclitaxel (cytotoxic agent), cyclopamine (hedgehog inhibitor), and

122 rast, the putative end-point metabolite, the cytotoxic agent des-acetyl vinblastine (1b), was ineffec

123 Although 99% of trials with cytotoxic agents determined an MTD, only 64% of trials w

124 , an antibody-drug conjugate composed of the cytotoxic agent DM1 conjugated to trastuzumab via a stab

125 e, an antibody-drug conjugate comprising the cytotoxic agent DM1 linked to trastuzumab, with treatmen

126 ), an antibody-drug conjugate comprising the cytotoxic agent DM1, a stable linker, and trastuzumab, h

127 (cisplatin), targeted agents (imatinib), and cytotoxic agents (docetaxel).

128 se the adjuvant therapy based on traditional cytotoxic agents does not act on either immune signaling

129 rve as magnetic hyperthermia agents and as a cytotoxic agent due to the known cobalt ion toxicity, al

130 ic amphipathic lytic peptides were chosen as cytotoxic agents due to their ability to depolarize mito

131 ading to the discovery of a number of potent cytotoxic agents (e.g., 27: GI50 = 51 nM against leukemi

132 cheduling strategies for anti-angiogenic and cytotoxic agents (either in monotherapy or in combinatio

133 improved pharmacokinetics, encapsulation of cytotoxic agents, enhanced accumulation of therapeutics

134 covery of a potent enantiospecific series of cytotoxic agents, exemplified by 4-methoxy-benzo[a]phena

135 e (6-MP) are effective immune modulators and cytotoxic agents extensively used in the treatment of au

136 ro study showed that idarubicin was the most cytotoxic agent for hepatocellular carcinoma (HCC) cell

137 vestigated, with some success, as a targeted cytotoxic agent for oncotherapy.

138 he introduction of the use of rapamycin as a cytotoxic agent for the treatment of DSRCT.

139 c drugs have been widely described as potent cytotoxic agents for cancer cells.

140 ld be tested in combination with traditional cytotoxic agents for recurrent and high-risk primary ped

141 optimal combinations of GSK3 inhibitors and cytotoxic agents for use in gliomas and other cancers.

142 quantities of a structurally dissimilar C30 cytotoxic agent, fredericamycin.

143 ance of the availability of all three active cytotoxic agents, FU-LV, irinotecan, and oxaliplatin, on

144 4 could be enhanced by combining it with the cytotoxic agent gemcitabine.

145 The quest for markers of sensitivity to cytotoxic agents has been ongoing for decades.

146 y profile of bevacizumab in combination with cytotoxic agents has not changed significantly, there ma

147 urthin B, a potent and differentially active cytotoxic agent, has been accomplished.

148 For many years cytotoxic agents have been developed to target apoptotic

149 Recently, specific cytotoxic agents have been shown to extend survival time

150 inations of antiangiogenic agents (AAs) with cytotoxic agents have shown significant promise in cance

151 with phlebotomies (low-risk patients) and/or cytotoxic agents (high-risk patients) and antiplatelet t

152 If so, ACVP should be a cytotoxic agent if properly delivered to the cancer cell

153 Malignant cells may evade death from cytotoxic agents if they are in a dormant state.

154 istant prostate cancer (CRPC), including new cytotoxic agents, immune-based therapies, circulating tu

155 gher activity as a microtubule inhibitor and cytotoxic agent in comparison with the parent structure.

156 nitric oxide (NO), a signaling molecule and cytotoxic agent in higher organisms.

157 NO is an essential cytotoxic agent in host defense, yet can be autotoxic if

158 ric oxide (NO), a key signaling molecule and cytotoxic agent in mammals.

159 chemotherapy was manageable and typical of a cytotoxic agent in patients with acute leukemia.

160 ining a putative antiangiogenic agent with a cytotoxic agent in patients with primary brain tumors.

161 the surface of cancer cells, but release the cytotoxic agent in the cytoplasm.

162 e by producing a higher concentration of the cytotoxic agent in the tumors.

163 ance, anti-recombination, and sensitivity to cytotoxic agents in a dam mutant background.

164 NX1 was upregulated posttranscriptionally by cytotoxic agents in C57BL/6 mice in vivo and hematopoiet

165 roenvironment for enhancement of efficacy of cytotoxic agents in cancer therapy.

166 makes caspase-8/9 activities susceptible to cytotoxic agents in glioma cells and that PTP1B plays a

167 preferred end point for phase III trials of cytotoxic agents in HRPC.

168 agents might potentially replace traditional cytotoxic agents in lymphoma.

169 is induced by interferon-beta (IFN-beta) and cytotoxic agents in NIH-OVCAR-3 ovarian carcinoma cells.

170 sensitive test to assess the activity of new cytotoxic agents in phase II studies.

171 th while continually producing and releasing cytotoxic agents in situ.

172 e been used as gene delivery vehicles and as cytotoxic agents in their own right by selective replica

173 of novel angular benzophenazines were potent cytotoxic agents in these cell lines and may be able to

174 increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting apoptosis, and de

175 for CPT sensitivity, but not for many other cytotoxic agents, in non-S-phase cells.

176 Other active cytotoxic agents include doxorubicin, ifosfamide, and da

177 nses 6 h following treatment with a range of cytotoxic agents including gamma-irradiation, cisplatin,

178 Patients had been administered various cytotoxic agents, including alkylating agents (240 patie

179 t in LNCaP) cells led to their resistance to cytotoxic agents, including docetaxel, mitoxantrone, eto

180 CLU is upregulated after exposure to various cytotoxic agents, including ionizing radiation (IR), lea

181 (Pgp) is an ATPase efflux pump for multiple cytotoxic agents, including vinblastine and colchicine.

182 tance to reactive oxygen species-induced and cytotoxic agent-induced stress by attenuating activation

183 ising strategy for cancer therapy, as direct cytotoxic agents, inducers of antitumor immune responses

184 Mutational signatures analysis showed how cytotoxic agents introduce hundreds of unique mutations

185 r functions, including resistance to several cytotoxic agents, iron homeostasis, and porphyrin transp

186 etylated lysine group to puromycin, a masked cytotoxic agent is created, which is serially activated

187 Resistance to cytotoxic agents is a major limitation for their clinica

188 ) the nonmyeloablative regimen together with cytotoxic agents is currently used especially for elderl

189 The usefulness of novel immunotherapies and cytotoxic agents is difficult to ascertain because of th

190 se of estramustine in combination with other cytotoxic agents is not recommended.

191 reason, and cytoablation with irradiation or cytotoxic agents is routinely used with the belief that

192 f cryptophycin 52 (2), an exceedingly potent cytotoxic agent, is described.

193 lass of therapeutics, consisting of a potent cytotoxic agent linked covalently to an antibody or anti

194 This gender difference in sensitivity to cytotoxic agents may be generalized to nonneuronal cells

195 gly, therefore, the toxicity of targeted and cytotoxic agents may differ in both clinical and radiolo

196 olymer structures that extend the release of cytotoxic agents may therefore increase survival and pre

197 -maytansine (DM1), a potent antimicrotubular cytotoxic agent, may provide targeted delivery of the dr

198 ked or conjugated to radioactive isotopes or cytotoxic agents, may prove useful in the therapy of inf

199 outcomes comparable with those that tested a cytotoxic agent (median RR, 5.1% [95% CI, 4.3%-6.0%] vs

200 these activities by conjugating to cAC10 the cytotoxic agent monomethyl auristatin E (MMAE) to create

201 activity in vitro, were conjugated with the cytotoxic agents monomethyl auristatin E (MMAE) or monom

202 otein scaffold (Fcmu) and linked it with the cytotoxic agent monomethylauristatin F.

203 evelop frequently in relapsed neuroblastoma, cytotoxic agents more sensitive to mutant p53 might be m

204 DNA-based cytotoxic agents: Nanopores composed of folded DNA featu

205 els, leaving cells susceptible to killing by cytotoxic agents normally exported by MRP1.

206 ng 2-deoxyglucose (2DG), in combination with cytotoxic agents on the induction of immunogenic cell de

207 not provide additional benefit compared with cytotoxic agents on their own.

208 velopment of early tumors and the effects of cytotoxic agents on tumors in vitro.

209 In KB 3-1 or Jurkat cells treated with cytotoxic agents or C6-ceramide, TcapQ647 detected apopt

210 is effect was not seen in cells treated with cytotoxic agents or unrelated inhibitors.

211 Initiation of anti-TNFalpha therapy, cytotoxic agents other than methotrexate (MTX), noncytot

212 ed by 2, and it increased the potency of the cytotoxic agents paclitaxel and 5-fluorouracil when give

213 on of HDAC1 in cancer cells treated with the cytotoxic agent parthenolide.

214 response, where activated microglia and its cytotoxic agents play a crucial pathologic role.

215 litaxel and carboplatin, addition of a third cytotoxic agent provided no benefit in PFS or OS after o

216 s that can predict response to commonly used cytotoxic agents provides opportunities to better use th

217 The 2,4'- and 4,4'-linked variants of the cytotoxic agent secalonic acid A and their analogues hav

218 Local iontophoretic delivery of cytotoxic agents should be considered for the treatment

219 rapy is utilization of antibodies to deliver cytotoxic agents specifically to antigen-expressing tumo

220 neered peptidyl pro-drug will release active cytotoxic agent strictly within the microenvironment of

221 In comparison to a standard cytotoxic agent such as doxorubicin (GI50 = 45.3 nM), 3

222 ate that in contrast to certain conventional cytotoxic agents such as ara-C, overexpression of Bcl-2

223 vels may be modest surrogates of response to cytotoxic agents such as docetaxel, but have not been va

224 rostate cancer, alone or in combination with cytotoxic agents such as docetaxel, or in other combinat

225 is exocytosis of lytic granules that contain cytotoxic agents such as perforin and granzyme.

226 rgets is exocytosis of granules that contain cytotoxic agents such as perforin and granzymes.

227 es, but did not affect the response to other cytotoxic agents such as TRAIL, etoposide, and cyclohexi

228 l line is deficient for apoptosis induced by cytotoxic agents such as UV, staurosporine, and thapsiga

229 ich N-type cells die in response to specific cytotoxic agents (such as cisplatin and doxorubicin) com

230 MCF-7/DX1 cells when co-administered with a cytotoxic agent, such as doxorubicin.

231 d in pG1 and further in pG1-S in response to cytotoxic agents, such as the proteasome inhibitor borte

232 Poor delivery and systemic toxicity of many cytotoxic agents, such as the recent promising combinati

233 baseline conditions, i.e. in the absence of cytotoxic agent, suggesting that tryptase has a homeosta

234 tivity of certain resistant strains to other cytotoxic agents suggests that our findings may point to

235 doxorubicin and salinomycin (a CSC-selective cytotoxic agent) synergized to kill cells expressing LMW

236 nt oral in vivo efficacy in potentiating the cytotoxic agent temozolomide in a B16F10 murine melanoma

237 port of GSH likely makes it a more effective cytotoxic agent than an inhibitor with a single mode of

238 tubulin polymerization and less active as a cytotoxic agent than tasidotin, cemadotin, and dolastati

239 Calicheamicin is a potent cytotoxic agent that causes double-strand DNA breaks, re

240 initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal mod

241 Cisplatin is a potent cytotoxic agent that functions as a bivalent electrophil

242 P3A7*1C allele, treatment of patients with a cytotoxic agent that is a CYP3A substrate, and clinical

243 Therefore, arming T cells with a cytotoxic agent that is capable of killing cancer cells

244 lated apoptosis-inducing ligand (TRAIL) is a cytotoxic agent that preferentially induces apoptosis in

245 ylase inhibitors may enhance the efficacy of cytotoxic agents that act by targeting DNA.

246 highly potent compounds could yield targeted cytotoxic agents that are effective treatments for many

247 recently, almost all cancer drugs were crude cytotoxic agents that discriminate poorly between cancer

248 hat the strategy of combining tumor-specific cytotoxic agents that function by differing mechanisms c

249 iviticin aglycon [aka: (-)-MK7-206, (3)] are cytotoxic agents that induce double-strand breaks (DSBs)

250 K-H deficient cells were hypersensitive to cytotoxic agents that induce DSBs, unable to reseal comp

251 baseline apoptosis, or sensitivity to other cytotoxic agents that target the mitochondria, cytoskele

252 If patients were receiving cytotoxic agents, the dosage was not increased.

253 Our strategy, which entails targeting of a cytotoxic agent, through a covalent enzyme inhibitor tha

254 ectable tumors through optical activation of cytotoxic agents, thus reducing many side effects associ

255 r, the in vivo administration of the hypoxic cytotoxic agent tirapazamine exhibited selective toxicit

256 B-CLL) were resistant to the novel selective cytotoxic agent, TNF-related apoptosis-inducing ligand (

257 ar antibodies (VAs) to selectively deliver a cytotoxic agent to tumor cells and exert potent inhibiti

258 The selective targeting of cytotoxic agents to a tumor has shown limited success by

259 matory agents, disease-modifying agents, and cytotoxic agents to address the extraglandular manifesta

260 ribed among the top 0.1% most-cell-selective cytotoxic agents to be evaluated in the NCI 60 cell line

261 ly be used in synergy with more conventional cytotoxic agents to bring about more immediate responses

262 y-drug conjugates that deliver highly potent cytotoxic agents to cancer cells for cancer therapy, we

263 the benefit of antibody-targeted delivery of cytotoxic agents to cancer cells.

264 ll-molecule inhibitors of IDO cooperate with cytotoxic agents to elicit regression of established tum

265 apidly screen radiopharmaceuticals and other cytotoxic agents to formulate more effective cocktails f

266 tibodies (MAbs) for their ability to deliver cytotoxic agents to infected or Env-transfected cells, w

267 treatments have evolved from indiscriminate cytotoxic agents to selective genome- and immune-targete

268 The precise targeting of cytotoxic agents to specific cell types or cellular comp

269 rexpression in GB tumors as a way to deliver cytotoxic agents to the glioma cells remaining after sur

270 e used for the selective pharmacodelivery of cytotoxic agents to the neoplastic mass.

271 to facilitate specific killing by confining cytotoxic agents to the synaptic cleft.

272 ternative approach is to selectively deliver cytotoxic agents to the tumor site.

273 Conjugation of cytotoxic agents to these nnAAs, yields homogeneous anti

274 Nanomedicines that preferentially deploy cytotoxic agents to tumors and molecular targeted therap

275 ssociated antigens have been used to deliver cytotoxic agents to tumour cells.

276 Targeted delivery of cytotoxic agents to tumours is believed to improve both

277 (NPC) expressing a secretable variant of the cytotoxic agent tumor necrosis factor-related apoptosis

278 thylating agent, and cytarabine, a frontline cytotoxic agent used in the treatment of AML, either alo

279 Genomic mutations caused by cytotoxic agents used in cancer chemotherapy may cause s

280 Traditional cytotoxic agents used in cancer therapy were initially d

281 he impact of RB depletion on the response to cytotoxic agents used to treat advanced disease.

282 o not confer resistance to several important cytotoxic agents used to treat neuroblastoma, we explore

283 ty of EGFR x c-MET bsAbs with the potency of cytotoxic agents via bispecific antibody-toxin conjugati

284 e development of peptidyl conjugate 5 of the cytotoxic agent vinblastine (1), along with the results

285 able but insignificant case cohort use among cytotoxic agents was found for exposure to cyclophospham

286 when antiangiogenic agents are combined with cytotoxic agents, we explored the clinical activity of t

287 tion strains are cross-resistant to selected cytotoxic agents whereas hypersensitive to others.

288 itional phase I, II, and III trials used for cytotoxic agents (which typically shrink tumors and in a

289 Thus, 9 may represent a promising cytotoxic agent, which is worthy of being further develo

290 eavage reaction intermediate is exploited by cytotoxic agents, which have important applications as a

291 ated with significantly poorer outcomes than cytotoxic agents, which in turn were worse than personal

292 ifferent mechanism of action than do classic cytotoxic agents, which predominantly attack rapidly pro

293 sensitivity of the deletion strains to other cytotoxic agents, which resulted in different drug-speci

294 er chemotherapy heavily relies on the use of cytotoxic agents, which typically do not preferentially

295 sphenazine anticancer drug MLN944 is a novel cytotoxic agent with exceptional anti-tumor activity aga

296 Bendamustine is a unique cytotoxic agent with structural similarities to alkylati

297 potent tubulin polymerization promoters and cytotoxic agents with (12R,13S,15S)-cyclopropyl 5-methyl

298 These compounds were potent cytotoxic agents with IC(50) values in the low micromola

299 compounds resulted in the identification of cytotoxic agents with potent activity toward both the Y7

300 ined tirapazamine (TPZ), a hypoxia-activated cytotoxic agent, with hepatic artery ligation (HAL), whi