<?xml version="1.0" encoding="UTF-8"?><rss xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:content="http://purl.org/rss/1.0/modules/content/" xmlns:atom="http://www.w3.org/2005/Atom" version="2.0"><channel><title><![CDATA[HuMax-IL8 licensed to Cormorant Pharmaceuticals]]></title><description><![CDATA[<p dir="auto">HuMax-IL8 licensed to Cormorant Pharmaceuticals</p>
<p dir="auto">Copenhagen, Denmark; May 30, 2012 — Genmab A/S (OMX: GEN) announced today it has granted an exclusive, worldwide license to its HuMax<img src="https://dev.proinvestor.com/forum/assets/plugins/nodebb-plugin-emoji/emoji/android/00ae.png?v=de222e39001" class="not-responsive emoji emoji-android emoji--registered" style="height:23px;width:auto;vertical-align:middle" title="®" alt="®" />-IL8 antibody to Cormorant Pharmaceuticals.  Under the terms of the agreement, Genmab will receive an upfront payment and will be entitled to milestone payments and royalties on net sales.  Cormorant intends to evaluate HuMax-IL8 for treatment of select cancers and will be responsible for all future costs of developing, manufacturing and commercializing HuMax-IL8.</p>
<p dir="auto">"We are pleased to enter this license agreement with Cormorant Pharmaceuticals who will work towards resuming the development of HuMax-IL8," said Jan van de Winkel, Ph.D., Chief Executive Officer of Genmab.</p>
<p dir="auto">This agreement does not affect Genmab's 2012 financial guidance.</p>
<p dir="auto">About HuMax-IL8<br />
HuMax-IL8 is a high affinity fully human IgG1,? antibody directed towards IL-8. IL-8 is a major mediator of inflammation, a potent chemoattractant for white blood cells called neutrophils, as well as an important factor in angiogenesis. HuMax-IL8 effectively blocks binding of IL-8 to neutrophils and inhibits neutrophils from migrating towards sites of inflammation via a process known as chemotaxis. HuMax-IL8 also potently inhibits IL-8 induced neutrophil activation. In pre-clinical studies, HuMax-IL8 has been shown to inhibit tumor growth in tumor models using primary human tumors in immunodeficient mice.</p>
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