Now showing items 1-4 of 4

    • The clinical development candidate CCT245737 is an orally active CHK1 inhibitor with preclinical activity in RAS mutant NSCLC and Eµ-MYC driven B-cell lymphoma. 

      Walton, MI; Eve, PD; Hayes, A; Henley, AT; Valenti, MR; De Haven Brandon, AK; Box, G; Boxall, KJ; Tall, M; Swales, K; Matthews, TP; McHardy, T; Lainchbury, M; Osborne, J; Hunter, JE; Perkins, ND; Aherne, GW; Reader, JC; Raynaud, FI; Eccles, SA; Collins, I; Garrett, MD (2016-01)
      CCT245737 is the first orally active, clinical development candidate CHK1 inhibitor to be described. The IC50 was 1.4 nM against CHK1 enzyme and it exhibited>1,000-fold selectivity against CHK2 and CDK1. CCT245737 potently ...
    • Induction of detrimental aneuploidy in basal breast cancer cells treated by MPS1 inhibitors in combination with paclitaxel 

      Anderhub, SJ; Mak, GWY; Faisal, A; Walsh, K; Gurden, M; Day, L; Innocenti, P; Woodward, HL; Westwood, IM; Cheung, K-MJ; Naud, S; Hayes, A; Box, G; de Haven Brandon, A; Valenti, MR; O'Fee, L; Saville, H; Burke, R; van Montfort, RLM; Raynaud, FI; Eccles, SA; Blagg, J; Hoelder, S; Linardopoulos, S (AMER ASSOC CANCER RESEARCH, 2017-07-01)
    • Orally bioavailable CDK9/2 inhibitor shows mechanism-based therapeutic potential in MYCN-driven neuroblastoma. 

      Poon, E; Liang, T; Jamin, Y; Walz, S; Kwok, C; Hakkert, A; Barker, K; Urban, Z; Thway, K; Zeid, R; Hallsworth, A; Box, G; Ebus, ME; Licciardello, MP; Sbirkov, Y; Lazaro, G; Calton, E; Costa, BM; Valenti, M; De Haven Brandon, A; Webber, H; Tardif, N; Almeida, GS; Christova, R; Boysen, G; Richards, MW; Barone, G; Ford, A; Bayliss, R; Clarke, PA; De Bono, J; Gray, NS; Blagg, J; Robinson, SP; Eccles, SA; Zheleva, D; Bradner, JE; Molenaar, J; Vivanco, I; Eilers, M; Workman, P; Lin, CY; Chesler, L (2020-10-05)
      The undruggable nature of oncogenic Myc transcription factors poses a therapeutic challenge in neuroblastoma, a pediatric cancer in which MYCN amplification is strongly associated with unfavorable outcome. Here, we show ...
    • Suppression of interferon gene expression overcomes resistance to MEK inhibition in KRAS-mutant colorectal cancer. 

      Wagner, S; Vlachogiannis, G; De Haven Brandon, A; Valenti, M; Box, G; Jenkins, L; Mancusi, C; Self, A; Manodoro, F; Assiotis, I; Robinson, P; Chauhan, R; Rust, AG; Matthews, N; Eason, K; Khan, K; Starling, N; Cunningham, D; Sadanandam, A; Isacke, CM; Kirkin, V; Valeri, N; Whittaker, SR (2019-03)
      Despite showing clinical activity in BRAF-mutant melanoma, the MEK inhibitor (MEKi) trametinib has failed to show clinical benefit in KRAS-mutant colorectal cancer. To identify mechanisms of resistance to MEKi, we employed ...