CytRx Corp. is a biopharmaceutical research and development oncology company based in Los Angeles, California.The CytRx oncology pipeline includes three programs in clinical development: bafetinib, tamibarotene and INNO-206. The company is evaluating bafetinib in the ENABLE Phase 2 clinical trial in high-risk B-cell chronic lymphocytic leukemia , a pharmacokinetic clinical trial in brain cancer and the PROACT Phase 2 clinical trial in advanced prostate cancer. With its tumor-targeting pro-drug candidate INNO-206, CytRx is conducting a safety trial with plans to initiate Phase 2 proof-of-concept clinical trials as a treatment for soft-tissue sarcomas and pancreatic cancer. CytRx's pipeline also includes tamibarotene, which it is testing in patients with non-small-cell lung carcinoma and which is in a registration clinical trial as a treatment for acute promyelocytic leukemia .Arimoclomol is an experimental drug developed by CytRx. The orally administered drug is intended to treat amyotrophic lateral sclerosis , also known as Lou Gehrig's Disease.Steven Arthur Kriegsman is the President and CEO. Wikipedia.
CytRx | Date: 2013-12-13
The invention relates to reconstituted formulations comprising an anthracycline compound, ethanol, and water. The invention also relates to injectable compositions comprising the reconstituted formulation and Lactated Ringers solution. Additionally, the invention relates to methods of using the formulations and compositions.
CytRx | Date: 2012-03-12
CytRx | Date: 2014-06-04
The present invention relates to a method of treating brain cancer comprising administering a therapeutically effective substance to a patient, wherein the therapeutically effective substance comprises: (I), or a pharmaceutically acceptable salt thereof, wherein X is a moiety that can be cleaved hydrolvtically or enzymaticaily in the body of the patient in a pH-dependent manner.
CytRx | Date: 2010-06-25
A method of increasing expression of a molecular chaperon by a cell and/or enhancing the activity of a molecular chaperon in cells is provided. The method comprises treating a cell that is exposed to a physiological stress which induces expression of a molecular chaperon by the cell with an effective amount of a certain hydroxylamine derivative to increase the stress. Alternatively, an hydroxylamine derivative can be administrated to a cell before it is exposed to a physiological stress which induces expression of a molecular chaperon by the cell. Preferably, the cell to which an hydroxylamine derivative is administered is an eukaryotic cell. The hydroxylamine derivative corresponds to the formulae (I) or (II). The invention also provides novel hydroxylamine derivatives falling within the scope of the formulae (I) and (II) as well as pharmaceutical and/or cosmetical compositions comprising the said compounds.
Agency: Department of Health and Human Services | Branch: | Program: SBIR | Phase: Phase I | Award Amount: 222.05K | Year: 2006
DESCRIPTION (provided by applicant): Type 2 diabetes (T2D) and obesity are major health concerns that have been increasing at an alarming rate over the last few decades resulting in costs to the medical system upwards of $100 billion annually in related medical expenses. Fatty acid synthase (FAS-1) is a key enzyme in mammals which regulates the de novo synthesis of saturated fatty acids such as palmitate and stearate. FAS plays an important role in energy homeostasis by converting excess caloric intake into lipids for storage and providing energy when needed via beta-oxidation. Elevation of plasma free fatty acid levels is an important clinical feature in T2D and obesity. Central inhibition of FAS-1 by the inhibitors cerulinin and C75 have been shown to suppress food intake, lead to dramatic weight loss and improved insulin responsiveness in mice. This Phase I SBIR grant proposes to exploit the recent findings that the FAS-1 beta-ketoacyl synthase (KS) and the thioesterase (TE) domains contain an active site triad which acts analogous to proteases in their mechanism of substrate cleavage. Using structure-based drug design and computational chemistry, we propose to design and synthesize focused transition-state inhibitory libraries against the TE and KS domains of human fatty acid synthase (FAS-1). The Specific Aims of this Phase I SBIR grant are: (1) using the recently published x-ray crystal structure of the TE domain of human FAS-1 to design and synthesize potent and specific transition-state compound inhibitory libraries with desirable drug-like properties, (2) to design and synthesize focused transition-state inhibitory libraries directed to the KS domain of human FAS-1 using an in-house generated high quality 3D homology model of the KS domain of human FAS-1, and (3) to test in enzyme and cellular assays these focused transition-state compound libraries to select potent inhibitors of FAS-1. Once enzyme inhibitors are identified, these hits will be screened in cell culture for their ability to inhibit cellular fatty acid synthesis and tested for selectivity and toxicity. The ultimate goal of this phase I grant is to advance a FAS-1 transition-state inhibitor to the lead optimization phase where upon Phase II funding we would: (a) clone and express human TE, (b) conduct co-crystallization studies on inhibitor/protein complexes, (c) model active inhibitors, (d) rationally design and synthesize potent and selective in vivo active FAS inhibitors, and (e) advance a clinical candidate based on positive results in in vivo efficacy models.