Cambridge, MA, United States

Anchor Therapeutics

www.anchortx.com
Cambridge, MA, United States
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News Article | November 16, 2016
Site: www.newsmaker.com.au

The report provides comprehensive information on the therapeutics under development for Type 2 Diabetes Disease, complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. The report also covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases. Additionally, the report provides an overview of key players involved in therapeutic development for Type 2 Diabetes Disease and features dormant and discontinued projects. The report helps in identifying and tracking emerging players in the market and their portfolios, enhances decision making capabilities and helps to create effective counter strategies to gain competitive advantage. Complete report on Type 2 Diabetes Disease - Pipeline Review, H2 2016 addition with 249 market data tables and 17 figures, spread across 1298 pages is available at http://www.reportsnreports.com/reports/747717-type-2-diabetes-pipeline-review-h2-2016.html This report features investigational drugs from across globe covering over 20 therapy areas and nearly 3,000 indications. The report is built using data and information sourced from Global Markets Directs proprietary databases, company/university websites, clinical trial registries, conferences, SEC filings, investor presentations and featured press releases from company/university sites and industry-specific third party sources. Drug profiles featured in the report undergoes periodic review following a stringent set of processes to ensure that all the profiles are updated with the latest set of information. Additionally, various dynamic tracking processes ensure that the most recent developments are captured on a real time basis Addex Therapeutics Ltd, Adocia ,Advinus Therapeutics Ltd ,Aegis Therapeutics, LLC ,AFFiRiS AG Alize Pharma SAS ,AlphaMab Co., Ltd ,Alteogen Inc. ,Amarantus Bioscience Holdings, Inc. ,Ambrx, Inc. ,Amgen Inc. ,Anchor Therapeutics, Inc. ,AntriaBio, Inc. ,Aphios Corporation ,APT Therapeutics, Inc. ,Araim Pharmaceuticals, Inc. ,Arisaph Pharmaceuticals, Inc. ,ArisGen SA ,Artery Therapeutics, Inc. ,Astellas Pharma Inc. ,AstraZeneca Plc ,Aus Bio Ltd ,Bayer AG ,Beta-Cell NV ,Betagenon AB,Biocon Limited ,Biodel Inc. ,Biogenomics Limited ,BioLingus AG ,BioRestorative Therapies, Inc. BioTherapeutics Inc. ,Biscayne Pharmaceuticals, Inc. ,Boehringer Ingelheim GmbH Inquire before buying http://www.reportsnreports.com/contacts/inquirybeforebuy.aspx?name=747717(This is a premium report price at US$2000 for a single user PDF license).


DeSimone C.V.,State University of New York at Buffalo | DeSimone C.V.,Mayo Medical School | Zarayskiy V.V.,State University of New York at Buffalo | Zarayskiy V.V.,Anchor Therapeutics | And 3 more authors.
Molecular Pharmacology | Year: 2011

Kv4 (Shal) potassium channels are responsible for the transient outward K+ currents in mammalian hearts and central nervous systems. Heteropoda toxin 2 (HpTx2) is an inhibitor cysteine knot peptide toxin specific for Kv4 channels that inhibits gating of Kv4.3 in the voltage-dependent manner typical for this type of toxin. HpTx2 interacts with four independent binding sites containing two conserved hydrophobic amino acids in the S3b transmembrane segments of Kv4.3 and the closely related Kv4.1. Despite these similarities, HpTx2 interaction with Kv4.1 is considerably less voltage-dependent, has smaller shifts in the voltage-dependences of conductance and steady-state in-activation, and a 3-fold higher Kd value. Swapping four non-conserved amino acids in S3b between the two channels exchanges the phenotypic response to HpTx2. To understand these differences in gating modification, we constructed Markov models of Kv4.3 and Kv4.1 activation gating in the presence of HpTx2. Both models feature a series of voltage-dependent steps leading to a final voltage-independent transition to the open state and closely replicate the experimental data. Interaction with HpTx2 increases the energy barrier for channel opening by slowing activation and accelerating deactivation. The greater degree of voltage-dependence in Kv4.3 occurs because it is the voltage-dependent transitions that are most affected by HpTx2; in contrast, it is the voltage-independent step in Kv4.1 that is most affected by the presence of toxin. These data demonstrate the basis for subtype-specificity of HpTx2 and point the way to a general model of gating modifier toxin interaction with voltage-gated ion channels. Copyright © 2011 The American Society for Pharmacology and Experimental Therapeutics.


Janz J.M.,Anchor Therapeutics | Ren Y.,Anchor Therapeutics | Looby R.,Anchor Therapeutics | Kazmi M.A.,Rockefeller University | And 13 more authors.
Journal of the American Chemical Society | Year: 2011

Cell surface heptahelical G protein-coupled receptors (GPCRs) mediate critical cellular signaling pathways and are important pharmaceutical drug targets.(1)In addition to traditional small-molecule approaches, lipopeptide-based GPCR-derived pepducins have emerged as a new class of pharmaceutical agents.(2, 3)To better understand how pepducins interact with targeted receptors, we developed a cell-based photo-cross-linking approach to study the interaction between the pepducin agonist ATI-2341 and its target receptor, chemokine C-X-C-type receptor 4 (CXCR4). A pepducin analogue, ATI-2766, formed a specific UV-light-dependent cross-link to CXCR4 and to mutants with truncations of the N-terminus, the known chemokine docking site. These results demonstrate that CXCR4 is the direct binding target of ATI-2341 and suggest a new mechanism for allosteric modulation of GPCR activity. Adaptation and application of our findings should prove useful in further understanding pepducin modulation of GPCRs as well as enable new experimental approaches to better understand GPCR signal transduction. © 2011 American Chemical Society.


Tchernychev B.,Anchor Therapeutics | Ren Y.,Anchor Therapeutics | Sachdev P.,Rockefeller University | Janz J.M.,Anchor Therapeutics | And 10 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2010

The G protein-coupled receptor (GPCR), chemokine CXC-type receptor 4 (CXCR4), and its ligand, CXCL12, mediate the retention of polymorphonuclear neutrophils (PMNs) and hematopoietic stem and progenitor cells (HSPCs) in the bone marrow. Agents that disrupt CXCL12-mediated chemoattraction of CXCR4-expressing cells mobilize PMNs and HSPCs into the peripheral circulation and are therapeutically useful for HSPC collection before autologous bone marrow transplantation (ABMT). Our aim was to develop unique CXCR4-targeted therapeutics using lipopeptide GPCR modulators called pepducins. A pepducin is a synthetic molecule composed of a peptide derived from the amino acid sequence of one of the intracellular (IC) loops of a target GPCR coupled to a lipid tether. We prepared and screened a small CXCR4-targeted pepducin library and identified several pepducins with in vitro agonist activity, including ATI-2341, whose peptide sequence derives from the first IC loop. ATI-2341 induced CXCR4-and G protein-dependent signaling, receptor internalization, and chemotaxis in CXCR4-expressing cells. It also induced dose-dependent peritoneal recruitment of PMNs when administered i.p. to mice. However, when administered systemically by i.v. bolus, ATI-2341 acted as a functional antagonist and dose-dependentlymediated release of PMNs from the bone marrow of both mice and cynomolgus monkeys. ATI-2341-mediated release of granulocyte/ macrophage progenitor cells from the bone marrow was confirmed by colony-forming assays. We conclude that ATI-2341 is a potent and efficacious mobilizer of bone marrow PMNs and HSPCs and could represent a previously undescribed therapeutic approach for the recruitment of HSPCs before ABMT.


Carlson K.E.,Anchor Therapeutics | McMurry T.J.,Anchor Therapeutics | Hunt S.W.,Anchor Therapeutics
Drug Discovery Today: Technologies | Year: 2012

Pepducins are a class of lipidated peptide G-protein coupled receptor (GPCR) allosteric modulators that exhibit unique pharmacological properties. Because of their rational design, pepducins can potentially be used to target all members of this gene family. In addition to enormous therapeutic potential, pepducins are proving to be valuable tools to elucidate the molecular mechanisms involved in GPCR signaling. In this review, we focus on the characterization of pepducin biology and discuss their utility as novel therapeutics. © 2011 Elsevier Ltd.


News Article | August 20, 2010
Site: www.xconomy.com

Anchor Therapeutics is developing first-in-class pepducin drug candidates, novel molecules that can selectively target G protein coupled receptors (GPCRs) to allosterically modulate GPCR signaling.


Patent
Anchor Therapeutics | Date: 2014-07-18

The invention relates generally to compounds which are allosteric modulators (e.g., negative and positive allosteric modulators, allosteric agonists, and ago-allosteric modulators) of the G protein coupled receptor apelin, also known as the APJ receptor. The APJ receptor compounds are derived from the it intracellular loop and domain of the APJ receptor. The invention also relates to the use of these APJ receptor compounds and pharmaceutical compositions comprising the APJ receptor compounds in the treatment of diseases and conditions associated with APJ receptor modulation, such as cardiovascular diseases, (e.g., hypertension and heart failure, such as congestive heart failure), cancer, diabetes, stem cell trafficking, fluid homeostasis, cell proliferation, immune function, obesity, metastatic disease, and HIV infection.


Patent
Anchor Therapeutics | Date: 2013-01-09

The invention relates generally to compounds which are allosteric modulators (e.g., negative and positive allosteric modulators, allosteric agonists, and ago-allosteric modulators) of the G protein coupled receptor apelin, also known as the APJ receptor. The APJ receptor compounds are derived from the it intracellular loop and domain of the APJ receptor. The invention also relates to the use of these APJ receptor compounds and pharmaceutical compositions comprising the APJ receptor compounds in the treatment of diseases and conditions associated with APJ receptor modulation, such as cardiovascular diseases, (e.g., hypertension and heart failure, such as congestive heart failure), cancer, diabetes, stem cell trafficking, fluid homeostasis, cell proliferation, immune function, obesity, metastatic disease, and HIV infection.


Trademark
Anchor Therapeutics and Ascent Therapeutics | Date: 2011-06-14

Biomedical compounds, namely, peptide screening agents for clinical or medical laboratory use in detecting or developing pharmaceutical preparations for treatment or prevention of diseases.


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