Bionomics and Merck Serono

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Bionomics and Merck Serono

Postby dignan » Sun Oct 12, 2008 10:00 am

Bionomics, a small Australian company trying to develop Kv1.3 inhibitors, signed a development agreement with Merck Serono in June.

Merck Serono and Bionomics Announce Multiple Sclerosis Development and Licensing Agreement

June 19, 2008

- Bionomics and Merck Serono to collaborate to discover and develop novel, oral treatment for MS
- Collaboration based on novel compounds that allow selective inhibition of the immune cells which cause nerve cell damage in patients with MS

Geneva, Switzerland, 19 June 2008 - Merck Serono, a division of Merck KGaA, Darmstadt, Germany, announced today that a Development and Licensing Agreement with Bionomics (ASX:BNO) was signed, under which Merck Serono would develop new treatments for multiple sclerosis (MS) and other autoimmune conditions based on compounds from Bionomics' Kv1.3 program.

Under the agreement, Bionomics will receive an upfront payment of US$2 million and committed research funding. Merck Serono will fund all development activities, including clinical development. Merck Serono intends to select compounds from Bionomics' pool of compounds, and for each compound selected by Merck Serono Bionomics may receive milestone payments of up to US$47 million, based on successful development and commercialization. In addition, Bionomics will be eligible to receive undisclosed royalties on the net sales of licensed products.

Dr Bernhard Kirschbaum, Executive Vice President Research at Merck Serono, said: "This partnership with Bionomics reflects our long-term commitment to patients with MS as Kv1.3 inhibition represents an innovative approach for the discovery of oral compounds in the field of MS. This R&D collaboration brings together Bionomics' expertise in Kv1.3 biology and Merck Serono's expertise in MS pharmacology in a combination that could speed up progress in the identification of novel drug candidates for the treatment of MS".

"As a world leader and pioneer in treatments for multiple sclerosis, Merck Serono is the ideal partner for Bionomics in this Kv1.3 program," commented Dr Deborah Rathjen, CEO and Managing Director of Bionomics. "The agreement with Merck Serono is an important milestone for our Company. It validates Bionomics' discovery approach, which has brought the program to this stage. We look forward to working with Merck Serono in the next stage to bring innovative treatment options for patients with MS to the clinic".

The compounds discovered by Bionomics, around which the collaboration will focus, target the potassium ion channel Kv1.3. Kv1.3 is a key modulator of the immune system and it is a target found on human immune cells which are associated with nerve cell damage in patients with MS. Inhibitors of Kv1.3 have been shown to inhibit the proliferation of these immune cells, suggesting that they have application in the treatment of MS and potentially other autoimmune conditions, including arthritis. ... 5&item=318

Some additional information: ... ts_319.pdf
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Postby Rita » Sun Oct 12, 2008 11:52 am

I remember that Kv1.3 was been studied by UC Irvine's College of Medicine in 2001. Now Merck Serono and Bionomics Announce that are going to develops it. I suppose they were thinking very carefully about it all this time.

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Postby dignan » Sun Oct 12, 2008 2:13 pm

Yep, the UC Irvine folks are still at it too...

Imaging of Effector Memory T Cells during a Delayed-Type Hypersensitivity Reaction and Suppression by Kv1.3 Channel Block.

Immunity. 2008 Oct 1.
Matheu MP, Beeton C, Garcia A, Chi V, Rangaraju S, Safrina O, Monaghan K, Uemura MI, Li D, Pal S, de la Maza LM, Monuki E, Flügel A, Pennington MW, Parker I, Chandy KG, Cahalan MD.
Department of Physiology and Biophysics and the Center for Immunology, University of California, Irvine, Irvine, CA 92697-4561, USA.

Effector memory T (Tem) cells are essential mediators of autoimmune disease and delayed-type hypersensitivity (DTH), a convenient model for two-photon imaging of Tem cell participation in an inflammatory response. Shortly (3 hr) after entry into antigen-primed ear tissue, Tem cells stably attached to antigen-bearing antigen-presenting cells (APCs). After 24 hr, enlarged Tem cells were highly motile along collagen fibers and continued to migrate rapidly for 18 hr.

Tem cells rely on voltage-gated Kv1.3 potassium channels to regulate calcium signaling. ShK-186, a specific Kv1.3 blocker, inhibited DTH and suppressed Tem cell enlargement and motility in inflamed tissue but had no effect on homing to or motility in lymph nodes of naive and central memory T (Tcm) cells. ShK-186 effectively treated disease in a rat model of multiple sclerosis. These results demonstrate a requirement for Kv1.3 channels in Tem cells during an inflammatory immune response in peripheral tissues. Targeting Kv1.3 allows for effector memory responses to be suppressed while central memory responses remain intact.

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