News

Food for Thought: Update on Germany´s Drug Reimbursement Law

Based on the latest developments in the debate about Germany´s new drug reimbursement law (AMNOG), we have updated our analysis, which was originally published in September 2010.  Please click here for the updated article.

Company News: SuppreMol closes C round, receives grant

Munich-based biotech company SuppreMol this month announced the closing of a EUR15.5 M C round as well as receiving a EUR1.6 M public research grant.

The money will be used for the GMP production and further clinical studies of its lead candidate SM101, a recombinant, soluble, non-glycosylated version of the Fc gamma receptor IIb. SM101, which has been granted orphan drug designation in the European Union and in the US, has already entered Phase Ib/IIa clinical studies in Primary Immune Thrombocytopenia (ITP), with interim results anticipated for next year. In addition, the company plans to initiate a Phase IIa study in Systemic Lupus Erythematosus (SLE) mid next year.

Moreover, SuppreMol will explore the therapeutic potential of  SM101 in Lupus Nephritis, a subcategory of this autoimmune disease affecting primarily the kidneys, and evaluate the compound in animal models for the treatment of Chronic Obstructive Pulmonary Disease (COPD). Last not least, the funds will be used for the preclinical development of an anti-FcgRIIb monoclonal antibody, which, due to the different properties of this molecule compared to SM101, may have beneficial therapeutic potential in certain autoimmune diseases.

The C round was led by MIG AG with BioMedPartners AG  as co-lead. The other existing investors Santo Holding GmbH, KfW Mittelstandsbank, Bayern Kapital GmbH and Max-Planck-Gesellschaft also participated in the round which was joined by FCP Biotech Holding GmbH as new investor.

Company News: Probiodrug to Host Alzheimer Symposium

Despite considerable efforts to find a cure, Alzheimer’s disease  (AD) at present cannot be treated adequately, as there is no therapy available to significantly slow down disease progression, halt the disease or prevent it.
During the past years, researchers from the German-based biotech company Probiodrug have generated a compelling body of evidence that a particular variant of the notorious A beta peptide, which clumps together in the brain of AD patients to the typical plaques, is the major culprit. This variant is formed through a hitherto unknown reaction of a brain enzyme called glutaminyl cyclase (QC) and carries a pyroglutamic residue at its N-terminus. This renders it much more neurotoxic than the unmodified A-beta and also significantly reduces its solubility so that it starts aggregating.
Today, this hypothesis  is not an outsider opinion any more. On Monday, November 22, well-known Alzheimer researchers from Germany (Christian Haass, Stephan v. Hörsten, Marcus Fändrich, Thomas Bayer, Steffen Roßner, and Stephan Schilling), the U.S. (Cynthia Lemere, Lennart Mucke, Steve Jacobsen), Austria (Reinhold Schmidt), and Japan (Takaomi Saido) will meet at Probiodrug´s Halle (Saale) headquarter to provide the latest findings in the light of this hypothesis and to discuss novel therapeutic strategies. One of the approaches pursued by Probiodrug is inhibiting the formation of the toxic A-beta variant by small molecule inhibitors of the QC enzyme.
The public symposium entitled “Neurodegenerative Disorders During Aging – Contemporary Research and New Therapies” will take place on Weinberg Campus in Halle (Saale) on Monday, November 22, 2010, from 10am to 3pm. The detailed program can be found on Probiodrug‘s website.

Food for Thought: Key to Stopping Alzheimer’s Disease

In Germany, newpapers are widely reporting about a recent paper by a team of researchers led by  Thomas Bayer from Ernst-August University Goettingen, Germany, in which the team reports about an approach able to halt the progress of Alzheimer’s disease in mice.

For a long time, researchers have tried to stop Alzheimer’s disease (AD) by either dissolving the plaques found in the brains of AD patients or by trying to get rid of the so-called Abeta peptide that is believed to aggregate to plaques. However, none of these approaches has been successful so far.

A couple of years ago, researchers from the biotech company Probiodrug AG (Halle, Germany) found that the major culprit for the detrimental aggregation of peptides to plaques is not Abeta as such, but a variation carrying a pyroglutamate residue. This pyroglutamated Abeta peptide (pGlu-Abeta), they found, is generated by a hitherto unknown reaction catalyzed by the brain enzyme glutaminyl cyclase (QC). pGlu-formation leads to stabilization of the peptide and protection against cleavage. Moreover, Probiodrug has been able to demonstrate that pGlu-Abeta peptides show increased neurotoxicity, a prolonged half-life and an increased tendency for aggregation. They also form the seeds of the typical plaques observed in the brain of AD patients.

While Probiodrug is developing small molecule inhibitors of the QC enzyme to halt the disease, Thomas Bayer (who is a member of Probiodrug’s Scientific Advisory Board) and his team generated a monoclonal antibody against pGlu-Abeta. Passive immunization of transgenic mice models of AD  with this monoclonal antibody significantly reduced overall Abeta plaque load and levels of pGlu-Abeta, and also normalized behavioral deficit in the mice.

Later this month during the Neuroscience 2010 conference, Probiodrug will demonstrate that increasing pGlu-Abeta potentiates the behavioral deficits observed with transgenic AD mouse models significantly, and will also presented data showing that inhibitors of QC can reduce the level of pyroglutamated beta-amyloid species and alleviate the observed behavioral changes.

While the approach presented by Thomas Bayer will take a few years to reach the clinic, Probiodrug’s first small molecule QC inhibitor already has reached the regulatory phase.

1 … 185 186 187 … 198