SCIRP Mobile Website
Paper Submission

Why Us? >>

  • - Open Access
  • - Peer-reviewed
  • - Rapid publication
  • - Lifetime hosting
  • - Free indexing service
  • - Free promotion service
  • - More citations
  • - Search engine friendly

Free SCIRP Newsletters>>

Add your e-mail address to receive free newsletters from SCIRP.

 

Contact Us >>

WhatsApp  +86 18163351462(WhatsApp)
   
Paper Publishing WeChat
Book Publishing WeChat
(or Email:book@scirp.org)

Article citations

More>>

J. A. Folkes, K. Ahmadi, K. Alderton, S. Alix, J. S. Baker, G. Box, S. Chuckowree, A. Clarke, P. Depledge, A. S. Eccles, S. Friedman, A. Hayes, C. Hancox, A. Kugendradas, L. Lensun, P. Moore, G. A. Olivero, J. Pang, S. Patel, H. G. Pergl-Wilson, I. F. Raynaud, A. Robson, N. Saghir, L. Salphati, S. Sohal, M. H. Ultsch, M. Valenti, H. J. Wallweber, N. C. Wan and C. Wiesmann, “The Identification of 2-(1H-indazol-4-yl)-6-(4-methanesulfonyl-piperazin-1-ylmethyl)-4-morpholin-4-yl-thieno[3,2-d]pyrimidine (GDC-0941) as a Potent, Selective, Orally Bioavailable Inhibitor of Class I PI3 Kinase for the Treatment of Cancer,” Journal of Medicinal Chemistry, Vol. 51, No. 18, 2008, pp. 5522-5532. doi:10.1021/jm800295d

has been cited by the following article:

  • TITLE: Molecular Docking of 4-Tert-buthyl-bis-(2,6-thiomorpholin-4-ylmethyl)-1-phenol (LQM319) on Fas Receptor (CD95)

    AUTHORS: Oscar Zuñiga, Víctor H. Vázquez, Ana María Velázquez, Víctor H. Abrego, Sandra Díaz-Barriga Arceo, Patricia Ramírez, Roberto Díaz, Enrique Angeles

    KEYWORDS: Fas Receptor (CD95); Fas Ligand (FasL); Docking

    JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.1, February 17, 2013

    ABSTRACT: The balance between cell proliferation and cell growth characterizes tissue homeostasis on one side and cell death on the other side. Fas receptor-mediated apoptosis is a control mechanism for tissue homeostasis, and avoiding this death pathway predisposes to many human diseases, including cancer. Current therapies for this disease are invasive and do not have the desired effect in the control of the disease. In this context, the search for new drugs that contribute to a better treatment is gaining more relevance. 4-tert-butyl-bis-(2,6-thiomorpholin-4-ylmethyl)-1-phenol (LQM319) [1,2] is a drug currently in preclinical stage, and we have shown that it has a hypertensive effect, similar to captopril, in a hypertensive rat model. Different studies have shown that some chemicals that are used as antihypertensive agents have an antineoplastic effect against certain types of cancer, as is the case of hydralazine [3], and captopril [4], among others [5]. On the other hand, it has been reported that morpholine derivatives may activate Fas (CD95)-mediated apoptosis. The aim of the present study was to show the interaction between CD95 (receptor) and thiomorpholine derivatives (ligand) using molecular modeling and docking studies, and to elucidate the possible action mechanism of 4-tert-butyl-bis-(2,6-thiomorpholin-4-ylmethyl)-1-phenol.