News Article | May 26, 2017
— Hypoparathyroidism - Pipeline Review, H1 2017 market research report adds on ReportsnReports.com store. The Hypoparathyroidism pipeline guide evaluates Hypoparathyroidism (Hormonal Disorders) therapeutics based on mechanism of action (MoA), drug target, route of administration (RoA) and molecule type. Browse Hypoparathyroidism Pipeline report has 7 Company Profiles, 14 Tables and 10 Figures, Spread across 43 Pages Report Available at http://www.reportsnreports.com/reports/1010771-hypoparathyroidism-pipeline-review-h1-2017.html . Hypoparathyroidism is decreased function of the parathyroid glands with underproduction of parathyroid hormone. This leads to low levels of calcium in the blood, often causing cramping and twitching of muscles (involuntary muscle contraction), and several other symptoms. The condition can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system-related damage as well as a number of rarer causes. The treatment includes artificial form of the hormone that can be administered as replacement, calcium replacement or vitamin. Main key players of Ulcerative Colitis are Ascendis Pharma A/S, Chugai Pharmaceutical Co Ltd, Eli Lilly and Company, Entera Bio Ltd, Pharis Biotec GmbH, Shire Plc Discount Available at http://www.reportsnreports.com/contacts/discount.aspx?name=1010771 (This report is available at upto 25% Discount till June 02nd 2017.) Hypoparathyroidism - Drug Profiles are hPTH-137, parathyroid hormone, PCO-371, PTH-RM, teriparatide. Hypoparathyroidism - Pipeline Review, H1 2017, provides comprehensive information on the therapeutics under development for Hypoparathyroidism (Hormonal Disorders), complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. The guide covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases. Hypoparathyroidism (Hormonal Disorders) pipeline guide 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. The guide is built using data and information sourced from 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. Additionally, various dynamic tracking processes ensure that the most recent developments are captured on a real time basis. Order a copy of this research report at http://www.reportsnreports.com/purchase.aspx?name=1010771 Scope - The pipeline guide provides a snapshot of the global therapeutic landscape of Hypoparathyroidism (Hormonal Disorders). The pipeline guide reviews pipeline therapeutics for Hypoparathyroidism (Hormonal Disorders) by companies and universities/research institutes based on information derived from company and industry-specific sources. The pipeline guide covers pipeline products based on several stages of development ranging from pre-registration till discovery and undisclosed stages. The pipeline guide reviews key companies involved in Hypoparathyroidism (Hormonal Disorders) therapeutics and enlists all their major and minor projects. The pipeline guide evaluates Hypoparathyroidism (Hormonal Disorders) therapeutics based on mechanism of action (MoA), drug target, route of administration (RoA) and molecule type. The pipeline guide encapsulates all the dormant and discontinued pipeline projects. The pipeline guide reviews latest news related to pipeline therapeutics for Hypoparathyroidism (Hormonal Disorders). Table of Contents Hypoparathyroidism - Overview Hypoparathyroidism - Therapeutics Development Pipeline Overview Pipeline by Companies Products under Development by Companies Hypoparathyroidism - Therapeutics Assessment Assessment by Target Assessment by Mechanism of Action Assessment by Route of Administration Assessment by Molecule Type Hypoparathyroidism - Companies Involved in Therapeutics Development Related Report Hypothyroidism - Pipeline Review, H1 2017 : The pipeline guide reviews key companies involved in Hypothyroidism (Hormonal Disorders) therapeutics and enlists all their major and minor projects. Companies Involved in Therapeutics Development: Genexine Inc, Synthonics Inc, Titan Pharmaceuticals Inc. About Us: ReportsnReports.com is an online market research reports library of 500,000+ in-depth studies of over 5000 micro markets. Call +1 888 391 5441 with your research requirements or email the details at email@example.com and we would be happy to help you find the business intelligence that you need. ReportsnReports.com offers research studies on agriculture, energy and power, automotive, Semiconductor and Electronics, Manufacturing & Construction, chemicals, environment, medical devices, healthcare, food and beverages, water and much more. For more information, please visit http://www.reportsnreports.com/reports/1010771-hypoparathyroidism-pipeline-review-h1-2017.html
Zirafi O.,University of Ulm |
Kim K.-A.,University of Ulm |
Standker L.,University of Ulm |
Standker L.,PHARIS Biotec GmbH |
And 36 more authors.
Cell Reports | Year: 2015
CXCL12-CXCR4 signaling controls multiple physiological processes and its dysregulation is associated with cancers and inflammatory diseases. To discover as-yet-unknown endogenous ligands of CXCR4, we screened a blood-derived peptide library for inhibitors of CXCR4-tropic HIV-1 strains. This approach identified a 16 amino acid fragment of serum albumin as an effective and highly specific CXCR4 antagonist. The endogenous peptide, termed EPI-X4, is evolutionarily conserved and generated from the highly abundant albumin precursor by pH-regulated proteases. EPI-X4 forms an unusual lasso-like structure and antagonizes CXCL12-induced tumor cell migration, mobilizes stem cells, and suppresses inflammatory responses in mice. Furthermore, the peptide is abundant in the urine of patients with inflammatory kidney diseases and may serve as a biomarker. Our results identify EPI-X4 as a key regulator of CXCR4 signaling and introduce proteolysis of an abundant precursor protein as an alternative concept for chemokine receptor regulation. © 2015 The Authors.
Forssmann W.-G.,Leibniz University of Hanover |
Forssmann W.-G.,VIRO Pharmaceuticals GmbH and Co. KG |
Forssmann W.-G.,Pharis Biotec GmbH |
The Y.-H.,Leibniz University of Hanover |
And 20 more authors.
Science Translational Medicine | Year: 2010
To infect host cells, most enveloped viruses must insert a hydrophobic fusion peptide into the host cell membrane. Thus, fusion peptides may be valuable targets for developing drugs that block virus entry. We have shown previously that a natural 20-residue fragment of a1-antitrypsin, designated VIRus-Inhibitory Peptide (VIRIP), that binds to the gp41 fusion peptide of HIV-1 prevents the virus from entering target cells in vitro. Here, we examine the efficacy of 10-day monotherapy with the optimized VIR-576 derivative of VIRIP in treatment-naïve, HIV-1-infected individuals with viral RNA loads of ≥10,000 copies per ml. We report that at the highest dose (5.0 grams per day), intravenous infusion of VIR-576 reduced the mean plasma viral load by 1.23 log10 copies per ml without causing severe adverse effects. Our results are proof of concept that fusion peptide inhibitors suppress viral replication in human patients, and offer prospects for the development of a new class of drugs that prevent virus particles from anchoring to and infecting host cells.
PubMed | Red Cross, Hannover Medical School, UMR7242, University of Pennsylvania and 7 more.
Type: Journal Article | Journal: Cell reports | Year: 2015
CXCL12-CXCR4 signaling controls multiple physiological processes and its dysregulation is associated with cancers and inflammatory diseases. To discover as-yet-unknown endogenous ligands of CXCR4, we screened a blood-derived peptide library for inhibitors of CXCR4-tropic HIV-1 strains. This approach identified a 16 amino acid fragment of serum albumin as an effective and highly specific CXCR4 antagonist. The endogenous peptide, termed EPI-X4, is evolutionarily conserved and generated from the highly abundant albumin precursor by pH-regulated proteases. EPI-X4 forms an unusual lasso-like structure and antagonizes CXCL12-induced tumor cell migration, mobilizes stem cells, and suppresses inflammatory responses in mice. Furthermore, the peptide is abundant in the urine of patients with inflammatory kidney diseases and may serve as a biomarker. Our results identify EPI-X4 as a key regulator of CXCR4 signaling and introduce proteolysis of an abundant precursor protein as an alternative concept for chemokine receptor regulation.
Agency: European Commission | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2012.2.3.2-3 | Award Amount: 6.60M | Year: 2012
Major advances in HIV/AIDS treatment regimens have fundamentally altered the natural history of the disease and sharply reduced HIV-related morbidity and mortality in countries where such treatments are accessible. The most notable advance is the use of combination antiretroviral therapy or ART. However, ART is unable to achieve virus eradication or sterilizing cure. Indeed, in most cases, viral rebound is observed after ART interruption. Thus, life-long treatment is currently needed to control HIV. Drug resistance, cumulative side effects and high cost, represent major drawbacks of such treatments. The persistence of HIV in treated patients results from the establishment of a viral reservoir insensitive to ART and poorly visible to the immune system. Thus, understanding HIV persistence and developing drugs able to flush out HIV, in order to achieve viral eradication or sterilizing cure remain outstanding challenges. Two main lines of research are being proposed. The first starts from the recent discovery by partners of this consortium of the immune-modulator Samhd1 as the cellular factor restricting HIV-1 infection in myeloid cells. We will explore a role for Samhd1 in immune activation and inflammation, and its impact on the balance between viral replication and persistence. To understand further HIV persistence, we will study the molecular mechanisms underlying post-integrative latency. The second aims at identifying and optimizing novel naturally occurring inducers of HIV reactivation. Additionally, a novel non-human primate model will be developed, allowing the study of viral persistence in vivo by tracking latently-infected cells. The project aims at (i) increasing knowledge on the contribution of immune activation and inflammation to HIV persistence (ii) deciphering the cellular and molecular mechanisms of viral persistence (iii) translating this basic knowledge into novel targets to achieve a cure for HIV/AIDS.
Dobrivojevic M.,University of Zagreb |
Sindic A.,University of Zagreb |
Edemir B.,Universitatsklinikum Munster |
Kalweit S.,Pharis Biotec GmbH |
And 2 more authors.
American Journal of Physiology - Cell Physiology | Year: 2012
In this study, the interaction of natriuretic peptides (NP) and bradykinin (BK) signaling pathways was identified by measuring membrane potential (Vm) and intracellular Ca2+ using the patch-clamp technique and flow cytometry in HEK-293 cells. BK and NP receptor mRNA was identified using RT-PCR. BK (100 nM) depolarized cells activating bradykinin receptor type 2 (B2R) and Ca2+-dependent Cl- channels inhibitable by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10 μM). The BK-induced Ca2+ signal was blocked by the B2R inhibitor HOE 140. [Des-Arg9]-bradykinin, an activator of B1R, had no effect on intracellular Ca2+. NP [atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and urodilatin] depolarized HEK-293 cells inhibiting K+ channels. ANP, urodilatin, BNP [binding to natriuretic peptide receptor (NPR)-A] and 8-bromo- (8-Br)-cGMP inhibited the BK-induced depolarization while CNP (binding to NPR-Bi) failed to do so. The inhibitory effect on BKtriggered depolarization could be reversed by blocking PKG using the specific inhibitor KT 5823. BK-stimulated depolarization as well as Ca2+ signaling was completely blocked by the phospholipase C (PLC) inhibitor U-73122 (10 nM). The inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenyl borate (2-APB; 50 μM) completely inhibited the BK-induced Ca2+ signaling. UTP, another activator of the PLC-mediated Ca2+ signaling pathway, was blocked by U-73122 as well but not by 8-Br-cGMP, indicating an intermediate regulatory step for NP via PKG in BK signaling such as regulators of G-protein signaling (RGS) proteins. When RGS proteins were inhibited by CCG-63802 in the presence of BK and 8-Br-cGMP, cells started to depolarize again. In conclusion, as natural antagonists of the B2R signaling pathway, NP may also positively interact in pathological conditions caused by BK. © 2012 the American Physiological Society.
Peigneur S.,Catholic University of Leuven |
Beress L.,Leibniz University of Hanover |
Beress L.,Pharis Biotec GmbH |
Moller C.,Florida Atlantic University |
And 4 more authors.
FASEB Journal | Year: 2012
APETx3, a novel peptide isolated from the sea anemone Anthopleura elegantissima, is a naturally occurring mutant from APETx1, only differing by a Thr to Pro substitution at position 3. APETx1 is believed to be a selective modulator of human ether-á-go-go related gene (hERG) potassium channels with a Kd of 34 nM. In this study, APETx1, 2, and 3 have been subjected to an electrophysiological screening on a wide range of 24 ion channels expressed in Xenopus laevis oocytes: 10 cloned voltage-gated sodium channels (NaV 1.2-NaV1.8, the insect channels DmNa V1, BgNaV1-1a, and the arachnid channel VdNaV1) and 14 cloned voltagegated potassium channels (KV1.1-K V1.6, KV2.1, KV3.1, KV4.2, K V4.3, KV7.2, KV7.4, hERG, and the insect channel Shaker IR). Surprisingly, the Thr3Pro substitution results in a complete abolishment of APETx3 modulation on hERG channels and provides this toxin the ability to become a potent (EC50 276 nM) modulator of voltage-gated sodium channels (NaVs) because it slows down the inactivation of mammalian and insect NaV channels. Our study also shows that the homologous toxins APETx1 and APETx2 display promiscuous properties since they are also capable of recognizing NaV channels with IC50 values of 31 nM and 114 nM, respectively, causing an inhibition of the sodium conductance without affecting the inactivation. Our results provide new insights in key residues that allow these sea anemone toxins to recognize distinct ion channels with similar potency but with different modulatory effects. Furthermore, we describe for the first time the target promiscuity of a family of sea anemone toxins thus far believed to be highly selective. © FASEB.
Pharis Biotec Gmbh | Date: 2012-08-03
A process for preparing human relaxin-2 having the following amino acid sequence: A chain: B chain: comprising the following steps: providing the amino acids necessary for the synthesis of the A and B chains with usual protective groups, wherein the cysteines are employed as trityl-protected amino acids (L-Cys(Trt)-OH); effecting a chromatographic purification of the individual chains A and B after the solid state synthesis; followed by the simultaneous folding and combination of the individual chains A and B in ammonium hydrogencarbonate buffer at pH 7.9 to 8.4; and subsequent purification of the relaxin-2 formed.
Pharis Biotec GmbH | Date: 2014-04-30
An N-terminally protected peptide having the sequence wherein X is a group protecting the N-terminal of the peptide.
Pharis Biotec Gmbh | Date: 2012-10-29
A peptide of the formula R^(1)-NH-HAEGTFTSDVSSYLEGQAAKEFIAWLVK-CONR^(2)R^(3 )wherein R=H or an organic compound comprising from 1 to 10 carbon atoms and R^(2 )R^(3)=independently H or an alkyl group of 1 to 4 carbon atoms; or certain analogues of said GLP-1 peptide can be used for the treatment and prophylaxis of heart ischemia-reperfusion injury