CoGenesys is seeking to outlicense a substantial intellectual property estate as well as lead molecules (antibodies and proteins) for 7 well-validated opportunities in both inflammation and oncology. These product opportunities are based on biologic mechanisms that are well validated in the literature. Each product is accompanied by patents and patent applications held by CoGenesys. Many of these targets offer the opportunity for development across multiple indications.
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HVEM-Fc for inflammation - One drug targeting both T and B cell mediated inflammation
HVEM-Fc inhibits T cell costimulation in a manner similar to CTLA4-Fc (Orencia® (abatacept), sold by BMS). HVEM-Fc has the potential for superior efficacy and therapeutic utility for a broader class of diseases because, acting through BTLA, HVEM-Fc inhibits both B and T cell proliferation. There are now numerous products in clinical development for autoimmune disease separately targeting the B cell and the T cell, illustrating the unique potential of HVEM-Fc. HVEM-Fc has a third, important inhibitory effect on a key pro-inflammatory pathway: it inhibits the role of another TNF family member in immune stimulation by preventing LIGHT/LTβR-mediated inflammation. LIGHT and antibodies to LIGHT are also available for licensing from CoGenesys (see below). Our data shows that HVEM-Fc inhibits T-cell costimulation, B-Cell proliferation and provides therapeutic benefit in murine models of disease. A lead Fc fusion protein and intellectual property on HVEM are available as part of a licensing package.
Anti-LIGHT for hepatitis and inflammatory bowel diseases - Ligand of HVEM, pro-inflammatory cytokine, target for IBD and hepatitis
LIGHT is a potent pro-inflammatory cytokine in theTNF ligand family. By preventing LIGHT/LTβR-mediated inflammation, LIGHT antagonism with HVEM-Fc or an antibody to LIGHT has been shown to provide therapeutic benefit in preclinical modes of autoimmune disease. LIGHT and antibodies to LIGHT are available for licensing from CoGenesys. LIGHT plays an especially important and therapeutically accessible role in gastrointestinal and liver inflammation and thus the LIGHT mAb is a unique opportunity for a new treatment for hepatitis and IBD. A lead monoclonal antibody and intellectual property on LIGHT are available as part of a licensing package.
Anti-CD200R for autoimmune disease and asthma - Strongly validated target for immune suppression in RA, transplant and other autoimmune diseases
Monoclonal antibodies against CD200R and soluble forms of CD200 (the ligand for CD200R), provide therapeutic reductions in inflammation associated with RA and substantial reductions in transplant rejection in mice [1-5]. Engagement of CD200R by its ligand or by agonist antibodies inhibits mast cell degranulation [6-10], down regulates the macrophage lineage , and reduces TH1 responses in vivo [2, 8, 11-14]. Abundant data support the utility of CD200R antibodies in development of a novel therapeutic for the treatment of autoimmune diseases, transplant rejection, and mast-cell dependent inflammatory conditions like asthma and allergy. A lead monoclonal antibody and intellectual property on CD200R are available as part of a licensing package.
Anti-CXCL16 for autoimmune disease - Target to treat inflammation in numerous tissues including, liver, lung, CNS, joint synovium and vasculature
The therapeutic rationale for development of an antibody to CXCL16 has recently been validated in a number of murine models: Antibody-mediated blockade of this chemokine provides therapeutic benefit in acute EAE, a murine model immunological liver injury, and in collagen-induced arthritis. CXCL16 is an interferon-gamma-regulated chemokine elevated in atherosclerotic plaques [1-3] and during inflammatory states in the liver [4-6], CNS , lung [8, 9] and joint synovium of patients with inflammatory disease [10, 11]. The severity of coronary artery stenosis was recently associated with a polymorphism in the CXCL16 gene  and it may play a role in inflammatory valvular heart disease . Also known as the scavenger receptor that binds phosphatidylserine and oxidized lipoprotein (SR-PSOX), CXCL16 is a membrane-bound and soluble chemokine expressed on macrophages and dendritic cells, while its receptor (CXCR6) is expressed on T and NK T cells. The interaction between SR-PSOX/CXCL16 and CXCR6 plays an important role in enhancing T cell responses by mature DCs in lymphoid tissues and in augmenting memory T cell responses by macrophages in peripheral inflamed tissues . Given the abundant recent evidence that CXCL16 plays an important and therapeutically accessible role in numerous inflammatory states, it is an excellent candidate for development of a novel biologic that could complement the growing list of successful biologics in the large and growing anti-inflammatory market. A lead monoclonal antibody and intellectual property on CXCL16 are available as part of a licensing package.
Anti-CXCR3 for autoimmune disease - Key target in T cell mediated inflammation, for treatment of autoimmune disease
CXCR3 plays a key role in T cell activation, allograft destruction, and recruitment to sites of inflammation in diseases like Crohn’s, MS, and RA. CoGenesys has developed a humanized CXCR3 antibody that blocks all three ligands of this receptor. As a T cell targeting therapy, anti-CXCR3 is expected to have anti-inflammatory properties in a broad class of autoimmune diseases. Because CXCR3 antagonism prevents effector T cell recruitment, but not naive T cell response, the antibody could reduce the tissue damage, swelling and pain associated with chronic inflammation without having the global immune-suppressive actions of conventional steroid treatments and anti-TNFs. Substantial validation exists for CXCR3 antagonism providing benefit in transplant rejection and other inflammatory conditions and provides strong support for clinical development of an antibody targeting CXCR3. A high-affinity humanized monoclonal antibody and intellectual property on CXCR3 are available as part of a licensing package.
Anti-TL1A for inflammatory bowel diseases - Target for treatment of inflammatory bowel disease
TL1A gene polymorphisms are strongly associated with high risk of Crohn’s disease in Japanese (P<10-10) and European IBD populations (p<0.02) . TL1A is a pro-inflammatory cytokine and a member of the TNF family . This protein exists in both membrane-bound and soluble forms and it is highly expressed in the inflamed bowel. TL1A is the only known ligand for death-domain receptor DR3 , which is primarily expressed on activated lymphocytes [2, 3]. Binding of TL1A to DR3 triggers proliferative activation signals [2, 4] specifically in memory T cells, but not naive T cells and TL1A potently induces secretion of IFN-g by human T cells [2, 5-7]. Moreover, both TL1A and DR3 are highy expressed in inflammatory bowel disease (IBD), particularly Crohn’s disease (CD) [6-13]. TL1A is also highly expressed in the joints of RA patients, where it may play a role in the T cell mediated inflammation (unpublished) and there is evidence that TL1A is up-regulated in response to toll receptor activation in the gut, where it likely participates in the initiation of IBD flares (unpublished). A lead monoclonal antibody and intellectual property on TL1A are available as part of a licensing package.
Anti-PD-L2 for oncology, asthma and vaccine enhancement - Stimulate antigen presentation, shift immune response to TH1, enhance vaccine efficacy
A naturally occurring human antibody potentiates dendritic cell function on cross-linking PD-L2 (aka B7-DC), supporting robust T cell responses to tumors [1-3]. This same antibody significantly inhibits allergic airway inflammation in a murine model of asthma [4-6]. The mechanism of action of this PD-L2 antibody involves multiple pathways initiated through PD-L2 expressed on dendritic cells. The outcome of the action of the PD-L2 antibody is augmented antigen presentation, enhanced NK T cell proliferation, antibody formation in response to antigen, and a shift from TH2 to TH1 phenotype in T cell populations in vivo. In different settings, these actions lead to reductions in allergic response and to augmentation of a natural anti-tumor response. Enhanced dendritic cell-mediated presentation of antigens by this antibody could also be exploited to enhance the potency of vaccines. We have generated a panel of fully human PD-L2 antibodies suitable for development as human therapeutics. A lead monoclonal antibody and intellectual property on PD-L2 are available as part of a licensing package.
References for Licensing Opportunities
HVEM References [Return to product summary]
LIGHT References [Return to product summary]
CD200R References [Return to product summary]
CXCL16 References [Return to product summary]
CXCR3 References [Return to product summary]
TL1A References [Return to product summary]
PD-L2 References [Return to product summary]
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