zur Startseite Food Mafia. Das Buch.
zur Startseite
zur Startseite

Terrorgefahr: Europas unsichere Sicherheitssysteme

Non fictional book unveals Daesh routes from Europe via UK to the US

Ich bin so frei: Willkommen im Lügenland


Link zur
OS-PLattform (ODR)


LifeGen.de Technology Transfer: Sie erfinden. Wir finden Investoren.

Aussenpolitik: Für ein neutrales Deutschland

Wie die Gesundheitspolitik das Leben suizidaler Kinder gefährdet

Gastbeitrag: Wie man die Target-Schulden tilgen kann

Orgasmus pur: Der G-Punkt als weibliche Prostata

Sinn und Scherben®: Clay Sculptures and Art News

Energiewende: GeneSys erzeugt in 3 Kilometer Tiefe Wärmetauscher

Hans-Werner Sinn: Gastbeitrag zur globalen Finanzkrise

Ehec: Interview mit IVI-Direktor Christian Griot

vfa Pharmabranche im Gespräch mit LifeGen.de

Porno-Branche im Visier der Seuchenforschung

Energiekrise: Wasserstoff macht Benzin und Diesel überflüssig

Klimawandel: Norddeutschland droht auf 430 Kilometern Länge in den Fluten zu versinken

Interview: Ein Quantencode bestimmt unser Leben nach dem Tod

Codierte Nano-Drähte entlarven Biowaffen

Neuromarketing nimmt Kinder ins Visier

Gefahren aus der Zwergenwelt

Auf der Suche nach dem Orgasmus-Hormon

Interview mit Prof. Rudi Balling, GBF

Die Jagd auf das 1000-Dollar Genom

Jens Reich im Gespräch mit LifeGen.de

Pflanzenviren auf dem Vormarsch

Chinas unaufhaltsamer Biotech-Aufstieg

Functional Food im Gartenbau:
Obst und Gemüse zwischen Hoffnung und Kommerz

LifeGen.de® is published by
London, UK



(c) 2001-2015 für alle Beiträge bei LifeGen.de®

Dieser Artikel ist kostenlos.

weitere kostenlose Artikel

Trophos increases focus on neuroprotection and cardioprotection

Trophos SA, a clinical stage pharmaceutical company developing innovative therapeutics for indications with under-served needs in neurology and cardiology, announced today that the company is increasing the focus of its development programs on neuroprotection and cardioprotection. The Company has a novel and proprietary cholesterol-oxime based pipeline of drug candidates that enhance the function and survival of stressed cells via modulation of dysfunctional mitochondria, through interactions at the permeability transition pore (mPTP). The announcement follows the award of nearly USD 9 million in grants associated with its lead drug candidate TRO19622

Advancing programs include:

MitoTarget: a Trophos led consortium has been awarded a EUR 6 million grant to study restorative approaches for therapy of neurodegenerative diseases, notably including support for a clinical efficacy study of TRO19622 in Amyotrophic Lateral Sclerosis (ALS) patients.

TRO40303: a second mitochondrial pore modulator, is scheduled to enter clinical development mid 2009 in cardiac ischemia-reperfusion injury. This innovative program has already been awarded a two year grant of nearly EUR 1million by the French Agence Nationale pour la Recherche (ANR) to support a project named IRIstop, which aims to further evaluate the ability of TRO40303, to arrest or prevent the cellular damage that occurs in preclinical models of both cardiac and cerebral ischemia-reperfusion injury

TRO19622: development in Spinal Muscular Atrophy (SMA), an orphan neurodegenerative disorder, continues following successful phase Ib study in SMA patients.

TRO19622: an exploratory phase IIa study in Chemotherapy (taxane)-induced peripheral neuropathy (CIPN) is to be initiated shortly. Taxane-induced neuropathies, which is a significant clinical issue for patients receiving such chemotherapy, are believed to be caused at least in part through a mechanism involving dysfunction of mitochondria and so may be amenable to treatment with TRO19622.

MS-Repair: a Trophos led collaboration has been awarded significant ANR grant to study the potential of its proprietary cholesterol-oxime compounds in in-vivo models of multiple sclerosis (MS).

Discontinued programs:

The phase IIa study of TRO19622 in diabetic neuropathic pain (DNP) showed excellent safety profile and was very well tolerated in this patient population but the primary endpoint of the trial was not met. Trophos will not pursue further development in this indication. The Company has also decided to halt a small, exploratory study in a liver condition, Non-Alcoholic SteatoHepatitis (NASH), due to high variability in the pre-treatment values for the primary end-point and will cease further work in this area.

A program of cost reductions is being implemented in all areas of the company to reduce operating expenses and minimize the need for additional financing as the company refocuses its resources on the greatest value-creation opportunities.

"We are delighted that the European Commission, after extensive expert evaluation, has chosen to support the MitoTarget project and are very pleased to be collaborating with a distinguished panel of academic and clinical investigators on furthering our understanding of the potential of this proprietary class of drug candidates, notably through the important ALS clinical trial that will take place with TRO19622," said Damian Marron, CEO at Trophos. "We are of course disappointed with the results of our DNP study and we are conducting additional analyses to gain further understanding, in particular relating to the placebo effect and profile of responders. However, the very good tolerability of the treatment augurs well for our future studies. We remain strongly convinced of the potential of mitochondrial pore modulation to bring much needed benefits in neurology and cardiology and we will be focusing our resources on our important clinical and research projects in these areas to create value for patients, the medical community and our investors."

Further details:

TRO40303: Pre-clinical results are very promising and mirror those of cyclosporine A, a known mitochondrial pore modulator that has recently shown efficacy in reducing infarct size in the clinic (Piot et al., NEJM 359:473-481, 2008). Reductions in infarct size of up to 40-50% have already been observed for TRO40303 in a dose-dependent manner in separate models run in separate laboratories.

The Company will continue its development programmed in SMA with TRO19622 following a phase Ib PK and tolerability study in SMA patients ranging from 6-25 years old, which demonstrated good tolerability and established the pharmacokinetic characteristics of the molecule in children. Discussions are ongoing with the EMEA regarding appropriate trial design to demonstrate efficacy and allow registration in this indication. This program has received financial support from the Association Française contre les Myopathies (AFM).

The exploratory phase IIa clinical trial of TRO19622 in chemotherapy induced peripheral neuropathy will include 40 patients. The primary end-points will be measures of dysesthesia and pain, and will also look for effects on nerve conduction velocity. Mitochondrial dysfunction is implicated in taxane-induced neuropathy (Flatters and Bennett, Pain 2006) and TRO19622 has demonstrated significant effects in reducing or preventing pain behavior and on the survival of intra-epidermal nerve fibers in pre-clinical models of taxane induced neurotoxicity. Results from this trial are expected around end of 2009.

Results of the phase IIa study of TRO19622 in diabetic neuropathic pain (DNP).

This randomized, double-blind, placebo-controlled, phase IIa clinical trial included 187 patients with painful peripheral diabetic neuropathy and compared the efficacy of a 500 mg dose of TRO19622 to placebo after 6 weeks of once-per-day oral treatment. The trial was performed in Europe at centers in Germany, Poland, Serbia, Croatia, and Latvia. TRO19622 demonstrated an excellent safety profile and was very well tolerated in this patient population. The primary endpoint of the trial, a significant decrease in mean pain score in the last week of treatment versus placebo as measured on the 11 point Likert scale on daily diary, was not met. It should be noted that pain intensity at baseline was somewhat lower than the norm for this type of study population, which may have impacted the ability of the study to detect efficacy. Further analyses are ongoing, including assessments of the placebo response, which appears higher than usual, and the profile of responders. Trophos will not pursue further development in this indication in order to focus on the most promising indications, as detailed elsewhere in this press release.

Preclinical results previously demonstrated the ability of TRO19622 to reverse the pain behavior in an experimental model of diabetic neuropathy (Bordet et al. JPET 2008). However, recent data shows this acute model may not reflect the pain syndrome associated with chronic diabetes in humans but may be more a model of chemo-toxicity (Pabbidi et al., Mol. Pharmacol. 73: 995-1004, 2008).

About Cardiac Ischemia Reperfusion Injury

Despite advances in treatment of myocardial infarction through removal of the occlusion, morbidity and mortality remain substantial, with about 5 to 6 per cent of patients having a subsequent cardiovascular event by 30 days. The abrupt reperfusion of ischemic myocardium can itself inflict injury on the myocardium, a phenomenon termed myocardial reperfusion injury. Experimental studies indicate that this form of myocardial injury accounts for up to 50 per cent of the final size of the infarct, providing an important potential target for protection of the heart (Hausenloy et al., NEJM359:5. 2008) and a recent clinical trial employing cyclosporine A support mitochondrial pore modulation as a therapeutic approach for cardiac ischemia reperfusion injury (Piot et al., NEJM 359:473-481, 2008).

About Spinal Muscular Atrophy:

Spinal Muscular Atrophy (SMA) is an autosomal recessive genetic disease that affects the motor neurons of the voluntary muscles that are used for activities such as crawling, walking, head and neck control, and swallowing. Approximately 1 in 6,000 babies born are affected and about 1 in 40 people are genetic carriers. SMA patients are divided into three subtypes depending on disease onset and severity but all suffer from degeneration of motor neurons controlling voluntary muscles with proximal limb and trunk muscle weakness leading to respiratory distress and in the most severe cases, ultimately death. For further information, see www.curesma.org

About Trophos: www.trophos.com

Trophos is a clinical stage pharmaceutical company developing innovative therapeutics for indications with under-served needs in neurology and cardiology. The Company has a novel and proprietary cholesterol-oxime based chemistry platform generating a pipeline of drug candidates, with a lead product, TRO19622, in phase II clinical trials. Trophos' mitochondrial pore modulator compounds enhance the function and survival of stressed cells via modulation of dysfunctional mitochondria through interactions at the permeability transition pore (mPTP). Recently published clinical studies support the therapeutic rationale for mitochondria targeted drugs in neurology (Alzheimer's disease) and cardiology (ischemia-reperfusion injury). Trophos is uniquely placed to exploit this validated therapeutic approach with its proprietary chemistry platform targeting the mitochondrial pore.

Für den Volltext-Zugang zu unseren Inhalten bitte mit Ihrem Usernamen/Passwort hier einloggen, wenn Sie bereits zahlender Abonnent von LifeGen.de sind.

Sie möchten alle unsere Inhalte lesen? Dann beziehen Sie einfach ein Abonnement. Bezahlen Sie einfach über Paypal, indem Sie den Buttom in der rechten Spalte anklicken. Die Zugangsdaten erhalten Sie dann via Email zugeschickt.



Passwort vergessen?
LifeGen.de abonnieren


LifeGen.de abonnieren

Member of The Internet Defense League

Deutscher Ethikrat


Universitätsklinikum Gießen
Universitätsbibliothek Bochum
Deutsche Zentralbibliothek für Medizin (ZB MED)
Net News Global
Transparency International
Deutschland e.V.


- kein Mainstream