MorphoSys Announces Completion of First Dosing in Phase 1 Trial for MOR103 Program

04/28/2008 at 07:30 AM

MorphoSys AG (FSE: MOR; Prime Standard Segment, TecDAX) today announced the completion of a first dosing regimen in a phase 1 clinical study on healthy volunteers of the HuCAL-derived antibody MOR103 with no adverse events reported. Six healthy volunteers in the first dosing group have been enrolled and received MOR103 injections, while three volunteers received placebo. The safety review of the medical data from the lowest dosing group yielded a determination that it was safe to proceed with the second dosing group. The randomized, double-blind, placebo-controlled, single-ascending dose trial will be conducted in approx. 50 healthy volunteers and is being conducted in a Clinical Pharmacology Unit (CPU) in Utrecht, the Netherlands. The trial is scheduled to be finalized in 2008 and final reporting is expected in Q1 2009.

The Company's lead development program, MOR103, is a fully human HuCAL antibody directed against GM-CSF (granulocyte macrophage-colony stimulating factor), being developed in the area of inflammatory diseases, such as rheumatoid arthritis, where current treatment options are inadequate. Due to its diverse functions in the immune system, GM-CSF can be considered a target for a broad spectrum of anti-inflammatory therapies. MorphoSys had submitted the clinical trial application in December 2007 and received the approval by the Dutch authorities six weeks later. The study will evaluate the safety and tolerability as well as pharmacokinetics of escalating doses of MOR103.

"We are very pleased to see our first proprietary drug candidate progress according to plan," commented Dr. Marlies Sproll, Chief Scientific Officer of MorphoSys AG. "Antibodies that neutralize GM-CSF could represent a new generation of medicines that reduce inflammation with greater beneficial effects."

For further information please contact: Dr. Claudia Gutjahr-Löser, Head of Corporate Communications & Investor Relations, Tel: +49 (0) 89 / 899 27-122, gutjahr-loeser@morphosys.com or Mario Brkulj, Manager Corporate Communications & Investor Relations, Tel: +49 (0) 89 / 899 27-454, brkulj@morphosys.com

About MorphoSys:
MorphoSys is a publicly traded biotechnology company focused on the generation of fully human antibodies as a means to discover and develop innovative antibody-based drugs against life-threatening diseases. MorphoSys's goal is to establish HuCAL as the technology of choice for antibody generation in research, diagnostics and therapeutic applications. The Company currently has therapeutic and research alliances with the majority of the world largest pharmaceutical companies including Boehringer Ingelheim, Centocor/Johnson & Johnson, Novartis, Pfizer and Roche. Within these partnerships, more than 50 therapeutic antibody programs are ongoing in which MorphoSys participates through exclusive license and milestones payments as well as royalties on any end products. Additionally, MorphoSys is active in the antibody research market through its AbD Serotec business unit. The business unit has operations in Germany (Munich), the U.S. (Raleigh, NC) and U.K. (Oxford). For further information please visit http://www.morphosys.com/


About MOR103 to treat RA:
Rheumatoid arthritis (RA) is traditionally considered a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints and affects in particular a membrane, called synovium, which lines each movable joint. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. As a systemic disease, RA often affects extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and muscles. The disease affects approximately 4-6 million people worldwide. In patients suffering from RA, white blood cells move from the bloodstream into the synovium. Here, these blood cells appear to play an important role in causing the synovial membrane to become inflamed. The HuCAL-based antibody MOR103 targets GM-CSF as a means to treat inflammatory diseases such as psoriasis, multiple sclerosis (MS), chronic obstructive pulmonary disease (COPD), asthma, and especially RA. The granulocyte macrophage colony-stimulating factor (GM-CSF) stimulates stem cells to produce granulocytes and macrophages, and subsequently activates these differentiated immune cells. GM-CSF is part of the natural immune and inflammatory cascade but has also been identified as an inflammatory mediator in autoimmune disorders like RA leading to an increased production of pro-inflammatory cytokines, chemokines and proteases and thereby ultimately to articular destruction. By neutralizing GM-CSF the HuCAL-based antibody MOR103 reduces undesired proliferation and activation of inflammatory granulocytes and macrophages and intervenes in several pathophysiological pathways. More information and picture material is available at: http://www.morphosys.com/en/mor103


HuCAL® and HuCAL GOLD® are registered trademarks of MorphoSys AG


This communication contains certain forward-looking statements concerning the MorphoSys group of companies. The forward-looking statements contained herein represent the judgment of MorphoSys as of the date of this release and involve risks and uncertainties. Should actual conditions differ from the Company's assumptions, actual results and actions may differ from those anticipated. MorphoSys does not intend to update any of these forward-looking statements as far as the wording of the relevant press release is concerned.

Micromet, Nycomed join forces on anti-GM-CSF antibodies

By Pete Mansell

29/05/2007 - Suppressing granulocyte macrophage colony-stimulating factor (GM-CSF) to tackle inflammatory and autoimmune diseases is the concept behind a new worldwide collaboration between German-American biopharmaceutical company Micromet and Denmark's Nycomed.

The agreement centres on Micromet's MT203, a human antibody expected to enter clinical trials in 2008. According to the new partners, MT203 neutralises GM-CSF, a cytokine known to play a significant role in autoimmune and inflammatory disease. Preclinical studies conducted by Micromet make a case for developing MT203 as a treatment for rheumatoid arthritis, multiple sclerosis, psoriasis, asthma and chronic obstructive pulmonary disease, they say.

Under the collaboration, Micromet will receive an upfront licence fee of €5m and additional payments and research and development (R&D) reimbursements of more than €120m in aggregate on achieving development milestones. The company is also eligible for royalties on worldwide sales of MT203 and any other products that may emerge from the agreement.

Micromet will take most of the responsibility for preclinical testing, process development and manufacturing of MT203 for early clinical trials, while Nycomed will be responsible for clinical development and commercialisation worldwide. Nycomed will also bear the cost of development activities and will reimburse Micromet for any expenses incurred in connection with the development programme.

Neutralising GM-CSF "presents a new biology concept in inflammatory processes and may have the potential to improve the lives of patients suffering from severe chronic inflammatory and autoimmune diseases," said Anders Ullman, Nycomed's executive vice-president R&D.

A human, high-affinity IgG1 antibody, MT203 was generated by Micromet using phage display-guided selection. The results of in vitro studies published last May in the journal Molecular Immunology showed that MT203 bound with picomolar affinity to an epitope on human and macaque GM-CSF involved in high-affinity receptor interaction.

As a consequence, the Micromet researchers said, the antibody potently prevented both GM-CSF-induced proliferation of TF-1 cells (these are used in proliferation bioassays for a number of cytokines and neutralising antibodies) and production of the chemokine IL-8 by U937 cells. MT203 significantly reduced both the survival and activation of peripheral human eosinophils, "as may be required for effective treatment of inflammatory lung diseases," they noted.

Another encouraging finding was that the antibody did not show any detectable loss of neutralising activity after five days in human serum at a temperature of 37°C.

In late June 2006, Micromet reported results from a study in arthritic mice challenged with streptococcus cell-wall fragments, in which a GM-CSF neutralising monoclonal was compared with the TNF (tumour necrosis factor)-alpha blocker etanercept, sold by Wyeth as Enbrel.

The monoclonal antibody (mAb) was found to be more potent than etanercept at reducing swelling of affected knee joints. While both the mAb and etanercept decreased the number of inflammatory cells in the joints, only the mAb cut levels of interleukin-1 beta (IL-1 beta) and reduced proteoglycan loss from the articular knee cartilage, Micromet pointed out.

IL1-beta mediates cartilage and bone destruction via secretion of metalloproteinases and decreases the synthesis of proteoglycan, one of the main components of the articular cartilage that cushions the body's joints.

These results suggested, therefore, that antibody neutralisation of GM-CSF might not only reduce inflammation but also protect cartilage from the destruction characteristic of arthritis - and that it might do so in TNF-alpha independent disease.

For Nycomed, the deal on MT203 highlights the company's strategic interest in inflammatory research and is the first example of its "strong commitment" to external collaborations at all stages of drug development as a key component of a new R&D strategy.

Following its acquisition of Germany's Altana Pharma in September 2006, Nycomed announced details earlier this year of an integration programme and strategic realignment that included redefining its R&D model to make it more flexible, results-oriented and "able to forge strong partnerships with external partners."