Genmab

J9302 (J-code) for Arzerra fra 2011: http://www.supercoder.com/articles/articles-alerts/onc/hcpcs-2011-j9302-j9307-and-j9315-offer-new-options-for-lymph-cancer-drugs/ http://www.reimbursementcodes.com/ Nu kommer salget.......

enkelt.....

som jeg sagde igår

Fortsættelse... Om IgG4-hingeless antibodies (Ny platform/antibody/Fab): Summary of the Results The data presented in the examples shows that expression of a hingeless IgG4 antibody by destroying the splice donor site of the hinge exon results in hingeless IgG4 half-molecules (one heavy and one light chain combined). The presence of IgG4 hingeless half-molecules is confirmed by SDS-PAGE under non-reducing conditions, mass spectrometry, size exclusion chromatography and radio immuno assay the absence of cross-linking abilities. The hingeless antibodies retain the same antigen binding specificity as natural format IgG1 and IgG4 antibody molecules. This is shown for two hingeless antibodies with different specificity, 7D8-HG (specific for the B-cell antigen CD20) and Betv1-HG (specific for the Birch pollen antigen Bet v 1). C1q binding of 7D8-HG is absent and only minor complement-dependent cellular toxicity (ADCC) is observed (comparable to the natural format 7D8-IgG4 antibody). Monovalency of the hingeless half-molecule is shown in the crosslinking experiment using Betv1-HG. Whereas both IgG1 and IgG4 show crosslinking of Sepharose bound Bet v 1 to radiolabelled Bet v 1, the hingeless molecule Betv1-HG is unable to crosslink. Half-life of 7D8-HG is evaluated in vivo in a mouse pharmacokinetic (PK) experiment and compared with 7D8-IgG4. Although 7D8-HG has a 2 to 3 times faster clearance than normal IgG4 in this model, the 6 day half-life is counted favorable to the half-life of less than one day reported for IgG F(ab?)2 fragments. We conclude that the favorable PK-profile will make IgG4-hingeless antibodies valuable for therapeutic applications when a non-crosslinking, monovalent and non-complement-activating antibody is needed. Om HIV: Our experiments provide proof-of-principle for an effective inhibition of HIV-1 infection of both CXCR4 and CCR5HIV-1 co-receptor expressing cells by monovalent binding of an anti-CD4 antibody (i.e. Fab fragment). This provides evidence that a similar inhibition could be accomplished by a HG anti-CD4 antibody osv. Den IgG4-hingelees antibdy er sandsynlig på R&D dagens agenda... Mon det ikke er denne variant eller varianter af et antibody patentet vedrørør - nyt link fra 23 dec 2010 http://www.faqs.org/patents/app/20100325744

En korrektion... IgG4 isotopen er Unibody og ikke Ultimab (IgG1) Unibody er altså en aktiv platform for Genmab med en aftale med Lundbeck og der arbejdes på flere targets bl.a. med anti-cd89 (astma) og C-Met der har følgende beskrivelse af funktionen: The receptor tyrosine kinase c-Met is prominently expressed on a wide variety of epithelial cells. During embryogenesis, cMet and Hepatocyte Growth factor/Scatter factor (HGF/SF) are involved in tissue-specific differentiation, leading to a proper organization of epithelial cells, muscle endothelium, and the nervous and hematopoietic systems. Abnormal cMet signalling has been implicated in tumorogenesis, particularly in the development of invasive and metastatic tumors. As a consequence of enhanced cMet activity, tumor cells may increase their growth rate and become resistant to apoptosis, resulting in a growth and/or survival advantage. Furthermore, cMet activation may lead to cytoskeletal reorganization and integrin activation, as well as to activation of proteolytic systems involved in extracellular matrix degradation, resulting in an increased invasive and metastatic capacity. Inhibition of HGF/SF-cMet signaling, therefore, represents an important therapeutic avenue for the treatment of malignant tumors. Afsnittet er i: Example 56 Proof of Concept Study with Hingeless IgG4 cMet (cMet-HG) Flere biotech arbejder på C-Met target bl.a. ARQL, EXEL og PFE

http://webcache.googleusercontent.com/search?q=cache:C1sRlDI-UpQJ:www.freepatentsonline.com/y2010/0306867.html+HuMab-7D8&cd=14&hl=da&ct=clnk&gl=dk For den der har god tid er der et nyligt opdateret patent fra Genmab. Genmab arbejder med: C-met target til prostata anti CD89 (IgG4/Ultimab) til inflammatoriske sygdomme f.ek. astma Tidliger nævnte Humab-7D8 (anto CD20 med effektiv bekæmpelse af B-celler der har lavt udtryk af CD20) TNX 101/Humax-CD4 til Hiv Mon ikke R&D dagen kommer med mere ! Har patentet til formål, at slippe ud af MEDX patentet ? Det har jeg ikke evner til at gennemskue.

Det kunne se ud til, at en ny anti-cd20 er på vej i klinisk - Humab-7D8. Meget effektiv i kombination med Ofatumumab http://www.haematologica.org/cgi/reprint/haematol.2010.025783v1.pdf GSK vil være med i den jf. deres aftale om udvikling imod CD-20 target.

Det var også min konklusion coller efter lidt resarch, men det kunne være jeg havde glippet et "smuthul"

Nu 51:(nyt ofatumumab studie) Ofatumumab In Older Patients With Untreated Low Or Intermediate Risk Indolent B-Cell Lymphomas This study is not yet open for participant recruitment. Verified by UNC Lineberger Comprehensive Cancer Center, December 2010 First Received: December 16, 2010 Last Updated: December 17, 2010

spændende med BP!

Skal den ikke bare hedde genamb?

Ganske pæn omtale af ofatumumab; http://updates.clltopics.org/2833-lenalidomide-in-the-news

BEGIVENHED DATO Offentliggørelse af årsregnskabsmeddelelse for 2010 Mandag den 28. februar 2011 Offentliggørelse af årsrapport for 2010 Onsdag den 15. marts 2011 Ordinær generalforsamling 2011 Onsdag den 6. april 2011 Offentliggørelse af kvartalsrapport for 1. kvartal 2011 Onsdag den 11. maj 2011 Offentliggørelse af halvårsrapport 2011 Onsdag den 3. august 2011 Offentliggørelse af kvartalsrapport for 3. kvartal 2011 Onsdag den 2. november 2011

Fra ASH: Identifying the Worst of the Worst and How Best to Treat Them Mark G. Frattini, MD, PhD December 6, 2010 In patients with CLL, Dr. Stephan Stilgenbauer from the University of Ulm in Ulm, Germany, described the ultra high-risk group as those with an expected overall survival of less than two to three years, patients with a chromosome 17p deletion or sole p53 mutation without 17p deletion, patients who are purine analog (i.e., fludarabine or pentostatin) refractory, and lastly those with only a 24- to 36-month remission duration following intensive therapy (e.g., FCR-fludarabine, cyclophosphamide, and rituximab). He stressed the need to treat these patients first-line on a clinical trial with novel agents. In addition, a consolidation strategy including either reduced-intensity allogeneic stem cell transplantation or clinical trial with novel agents should be considered depending on patient age and performance status. In the absence of a clinical trial with novel agents, immunotherapy with ofatumumab or alemtuzumab or other chemoimmunotherapy could be used.

chr.: ofte kommer der en chance til og så har man set om det bliver knald eller fald

syndes genmab se rigtigt ud har bemærket csb har købt en del de sidste dage

Så er der jo "jubilæum" - forsøg nr 50 Mon ikke vi skulle lave en oversigt over alle forsøgene ?

ja buler

Exitpling

Nyt studie med Ofatumumab: The goal of this clinical research study is to find out if ofatumumab can control Chronic Lymphocytic Leukemia (CLL) or Small Lymphocytic Lymphoma (SLL) that is left after chemotherapy or chemoimmunotherapy. The safety of the drug will also be studied. Ofatumumab for Minimal Residual Disease (MRD) and Maintenance Therapy This study is not yet open for participant recruitment. Verified by M.D. Anderson Cancer Center, December 2010 First Received: December 9, 2010 Last Updated: December 10, 2010 http://clinicaltrials.gov/ct2/show/NCT01258933?term=ofatumumab&rank=24