Jeg faldt over dette abstract hertil morgen. Jeg savner ganske enkelt forudsætninger for at vurdere dets betydning, derfor denne post. Umiddelbart er der elementer der ser det lovende ud... jeg tænker navnlig på den åbne overlevelse!
Clin Lymphoma Myeloma. 2009 Dec;9(6):E36.
Ofatumumab, a Novel CD20 Monoclonal Antibody, Is Active in Patients With Fludarabine- and Alemtuzumab-Refractory or Bulky Fludarabine-Refractory Chronic Lymphocytic Leukemia Irrespective of Prior Rituximab.
Wierda W, Kipps T, Mayer J, Stilgenbauer S, Williams CD, Hellmann A, Robak T, Furman RR, Hillmen P, Trneny M, Dyer MJ, Padmanabhan S, Piotrowska M, Kozak T, Chan G, Davis R, Losic N, Wilms J, Russell C, Osterborg A.
The University of Texas, M. D. Anderson Cancer Center, Houston.
Ofatumumab, a novel CD20 monoclonal antibody, produces high response rates regardless of prior rituximab exposure in patients with fludarabine- and alemtuzumab-refractory or bulky fludarabine-refractory chronic lymphocytic leukemia.Background: Patients with CLL refractory to fludarabine and alemtuzumab (FA-ref ) or refractory to fludarabine with bulky (> 5 cm) lymphadenopathy (BF-ref ) have poor outcomes with current salvage therapy (overall response rate [ORR], 23%; overall survival [OS], 9 months). Ofatumumab is a human monoclonal antibody that binds a distinct membrane-proximal epitope on the CD20 molecule and elicits more efficient in vitro complement-dependent cytotoxicity of B-cell lines and primary tumor cells versus rituximab. We assessed whether prior rituximab exposure impacted outcomes with ofatumumab in patients with FA-ref or BF-ref CLL enrolled in an international, pivotal trial. Patients and Methods: Patients received 8 weekly ofatumumab infusions followed by 4 monthly infusions (infusion, 1300 mg; infusions 2-12, 2000 mg). The primary endpoint was ORR (1996 NCI-WG criteria) assessed by an Independent Endpoint Review Committee over 24 weeks. Secondary efficacy endpoints included progression-free survival (PFS) and OS. Results: In the 59 FA-ref and 79 BF-ref patients at the planned interim analysis, ORR was 58% (95% CI, 40%-74%) and 47% (95% CI, 32%-62%), respectively. Median PFS was 5.7 months (95% CI, 4.5-8.0 months) and 5.9 months (95% CI, 4.9-6.4 months), and median OS was 13.7 months (95% CI, 9.4-[not yet reached] months) and 15.4 months (95% CI, 10.2-20.2 months), respectively. In the subgroup of FA-ref (n = 35) and BF-ref (n = 43) patients who previously received a rituximab-containing regimen, ORR was 54% and 44%, and median PFS was 5.5 months (95% CI, 3.7-8.0 months) and 5.5 months (95% CI, 3.8-6.4 months), respectively. In FA-ref and BF-ref patients refractory to fludarabine in combination with rituximab and cyclophosphamide (n = 16 in each group), ORR was 50% and 44%, and median PFS was 4.6 months (95% CI, 2.3-6.4 months) and 5.6 months (95% CI, 2.1-6.6 months), respectively.
Conclusion: Single-agent ofatumumab is active in patients with FA-ref and BF-ref CLL, irrespective of prior anti-CD20 monoclonal antibody therapy with rituximab, including refractoriness to fludarabine-based regimens containing rituximab.
http://www.ncbi.nlm.nih.gov/pubmed/19951868?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1
Clin Lymphoma Myeloma. 2009 Dec;9(6):E36.
Ofatumumab, a Novel CD20 Monoclonal Antibody, Is Active in Patients With Fludarabine- and Alemtuzumab-Refractory or Bulky Fludarabine-Refractory Chronic Lymphocytic Leukemia Irrespective of Prior Rituximab.
Wierda W, Kipps T, Mayer J, Stilgenbauer S, Williams CD, Hellmann A, Robak T, Furman RR, Hillmen P, Trneny M, Dyer MJ, Padmanabhan S, Piotrowska M, Kozak T, Chan G, Davis R, Losic N, Wilms J, Russell C, Osterborg A.
The University of Texas, M. D. Anderson Cancer Center, Houston.
Ofatumumab, a novel CD20 monoclonal antibody, produces high response rates regardless of prior rituximab exposure in patients with fludarabine- and alemtuzumab-refractory or bulky fludarabine-refractory chronic lymphocytic leukemia.Background: Patients with CLL refractory to fludarabine and alemtuzumab (FA-ref ) or refractory to fludarabine with bulky (> 5 cm) lymphadenopathy (BF-ref ) have poor outcomes with current salvage therapy (overall response rate [ORR], 23%; overall survival [OS], 9 months). Ofatumumab is a human monoclonal antibody that binds a distinct membrane-proximal epitope on the CD20 molecule and elicits more efficient in vitro complement-dependent cytotoxicity of B-cell lines and primary tumor cells versus rituximab. We assessed whether prior rituximab exposure impacted outcomes with ofatumumab in patients with FA-ref or BF-ref CLL enrolled in an international, pivotal trial. Patients and Methods: Patients received 8 weekly ofatumumab infusions followed by 4 monthly infusions (infusion, 1300 mg; infusions 2-12, 2000 mg). The primary endpoint was ORR (1996 NCI-WG criteria) assessed by an Independent Endpoint Review Committee over 24 weeks. Secondary efficacy endpoints included progression-free survival (PFS) and OS. Results: In the 59 FA-ref and 79 BF-ref patients at the planned interim analysis, ORR was 58% (95% CI, 40%-74%) and 47% (95% CI, 32%-62%), respectively. Median PFS was 5.7 months (95% CI, 4.5-8.0 months) and 5.9 months (95% CI, 4.9-6.4 months), and median OS was 13.7 months (95% CI, 9.4-[not yet reached] months) and 15.4 months (95% CI, 10.2-20.2 months), respectively. In the subgroup of FA-ref (n = 35) and BF-ref (n = 43) patients who previously received a rituximab-containing regimen, ORR was 54% and 44%, and median PFS was 5.5 months (95% CI, 3.7-8.0 months) and 5.5 months (95% CI, 3.8-6.4 months), respectively. In FA-ref and BF-ref patients refractory to fludarabine in combination with rituximab and cyclophosphamide (n = 16 in each group), ORR was 50% and 44%, and median PFS was 4.6 months (95% CI, 2.3-6.4 months) and 5.6 months (95% CI, 2.1-6.6 months), respectively.
Conclusion: Single-agent ofatumumab is active in patients with FA-ref and BF-ref CLL, irrespective of prior anti-CD20 monoclonal antibody therapy with rituximab, including refractoriness to fludarabine-based regimens containing rituximab.
http://www.ncbi.nlm.nih.gov/pubmed/19951868?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1
Lidt Keywords fra en rapport som koster 11K dollars....
10/12 2009 13:53 tumult 0
23313 Køb!
Den vil vi geren se.
Iøvrigt,- MA20 nærmer sig aktuel kurs. Nu i 82.
Spændende om den kan brydes, eller den lige som tidligere virker som "låg".
Den vil vi geren se.
Iøvrigt,- MA20 nærmer sig aktuel kurs. Nu i 82.
Spændende om den kan brydes, eller den lige som tidligere virker som "låg".
For en særdeles grundig! gennemgang og analyse, se denne (så jo - nogle tror stadig på potentialet):
http://informahealthcare.com/doi/pdf/10.1517/13543780902832679
http://informahealthcare.com/doi/pdf/10.1517/13543780902832679
11/12 2009 16:07 collersteen 023365 http://www.marketwatch.com/story/biogen-roche-report-study-results-for-ra-drug-2009-12-11
Gode resultater... men bivirkninger...?
Hvad får I ud af det?
Her er hele pressemeddelelsen
http://www.marketwatch.com/story/genentech-and-biogen-idec-announce-positive-results-from-first-phase-iii-trial-of-ocrelizumab-in-rheumatoid-arthritis-2009-12-11
Gode resultater... men bivirkninger...?
Hvad får I ud af det?
Her er hele pressemeddelelsen
http://www.marketwatch.com/story/genentech-and-biogen-idec-announce-positive-results-from-first-phase-iii-trial-of-ocrelizumab-in-rheumatoid-arthritis-2009-12-11
Tjaaa. HVad kan man slutte ud af det. Det er ikke givet at de selv tror på Ocrelizumab i RA. Bivirkninger er virkeligt noget FDA også kigger på, så er det værd at file på?
Men de har jo allerede omsætning på Rituxian i RA, men de føler sig måske ikke sikker på at den kan holde omsætningen eller at et CD2o stof er det rigtige.
Men de har jo allerede omsætning på Rituxian i RA, men de føler sig måske ikke sikker på at den kan holde omsætningen eller at et CD2o stof er det rigtige.
Binding of Submaximal C1q Promotes Complement-Dependent Cytotoxicity (CDC) of B Cells Opsonized with Anti-CD20 mAbs Ofatumumab (OFA) or Rituximab (RTX):
Considerably Higher Levels of CDC Are Induced by OFA than by RTX1
Andrew W. Pawluczkowycz*, Frank J. Beurskens, Paul V. Beum*, Margaret A. Lindorfer*, Jan G. J. van de Winkel,, Paul W. H. I. Parren and Ronald P. Taylor2,*
* Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908; Genmab, Utrecht, The Netherlands; and Immunotherapy Laboratory, Department of Immunology, University Medical Center, Utrecht, The Netherlands
The CD20 mAb ofatumumab (OFA) is more effective than rituximab (RTX) in promoting complement-dependent cytotoxicity (CDC) of B cells via the classical pathway (CP) of complement.
CP activation is initiated by C1q binding to cell-bound IgG. Therefore, we examined the role of C1q in the dynamics of complement activation and CDC of B cell lines and primary cells from patients with chronic lymphocytic leukemia, reacted with OFA or RTX. C1q binding, complement activation, and colocalization of C1q with cell-bound mAbs were determined by flow cytometry and high-resolution digital imaging. C1q binds avidly to OFA-opsonized Raji and Daudi cells (KD = 12?16 nM) and colocalizes substantially with cell-bound OFA. Cells opsonized with OFA undergo high levels of complement activation and CDC in C1q-depleted serum supplemented with low concentrations of C1q. Under comparable conditions, RTX-opsonized cells bind less C1q; in addition, even when higher concentrations of C1q are used to achieve comparable C1q binding to RTX-opsonized cells, less complement activation and CDC are observed. Greater CDC induced by OFA may occur because C1q is bound in close proximity and with high avidity to OFA, resulting in effective CP activation. Moreover, OFA binds to the small, extracellular CD20 loop, placing the mAb considerably closer to the cell membrane than does RTX. This may facilitate effective capture and concentration of activated complement components closer to the cell membrane, potentially shielding them from inactivation by fluid phase agents and promoting efficient generation of the membrane attack complex.
Considerably Higher Levels of CDC Are Induced by OFA than by RTX1
Andrew W. Pawluczkowycz*, Frank J. Beurskens, Paul V. Beum*, Margaret A. Lindorfer*, Jan G. J. van de Winkel,, Paul W. H. I. Parren and Ronald P. Taylor2,*
* Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908; Genmab, Utrecht, The Netherlands; and Immunotherapy Laboratory, Department of Immunology, University Medical Center, Utrecht, The Netherlands
The CD20 mAb ofatumumab (OFA) is more effective than rituximab (RTX) in promoting complement-dependent cytotoxicity (CDC) of B cells via the classical pathway (CP) of complement.
CP activation is initiated by C1q binding to cell-bound IgG. Therefore, we examined the role of C1q in the dynamics of complement activation and CDC of B cell lines and primary cells from patients with chronic lymphocytic leukemia, reacted with OFA or RTX. C1q binding, complement activation, and colocalization of C1q with cell-bound mAbs were determined by flow cytometry and high-resolution digital imaging. C1q binds avidly to OFA-opsonized Raji and Daudi cells (KD = 12?16 nM) and colocalizes substantially with cell-bound OFA. Cells opsonized with OFA undergo high levels of complement activation and CDC in C1q-depleted serum supplemented with low concentrations of C1q. Under comparable conditions, RTX-opsonized cells bind less C1q; in addition, even when higher concentrations of C1q are used to achieve comparable C1q binding to RTX-opsonized cells, less complement activation and CDC are observed. Greater CDC induced by OFA may occur because C1q is bound in close proximity and with high avidity to OFA, resulting in effective CP activation. Moreover, OFA binds to the small, extracellular CD20 loop, placing the mAb considerably closer to the cell membrane than does RTX. This may facilitate effective capture and concentration of activated complement components closer to the cell membrane, potentially shielding them from inactivation by fluid phase agents and promoting efficient generation of the membrane attack complex.
Rytter skylder nok et svar, refrac tallene for Arzerra var intet mindre end verdensklasse. Der kan ikke siges nok om det imponerende resultat i patienter der har fejlet andre behandlinger. Men nu sidder alle og vente på salgstallene i denne indikation.
Update in the management of chronic lymphocytic leukemia.
Maddocks KJ, Lin TS.
The Ohio State University, Division of Hematology-Oncology, 320 West 10th Avenue, Columbus, Ohio 43210, USA. lin.563@osu.edu.
ABSTRACT: Advances in the treatment of chronic lymphocytic leukemia (CLL) have improved initial overall response (OR) rates, complete response (CR) rates and progression free survival (PFS). Despite these advances, CLL remains incurable with standard therapies. Thus, there remains a need for more effective therapies in both the upfront and relapsed setting, particularly for patients with high-risk cytogenetic abnormalities such as del(11q22) and del(17p13). The 2008 American Society of Hematology (ASH) Annual Meeting featured several presentations which highlighted the ongoing clinical advances in CLL. The benefit of adding rituximab to purine analog therapy in the upfront setting was demonstrated by a large randomized study which showed that the addition of rituximab to fludarabine and cyclophosphamide (FCR) significantly improved OR, CR and PFS. The improvement in PFS directly resulted from an improved ability to eliminate minimal residual disease (MRD) in the peripheral blood, highlighting the importance of MRD eradication. However, a multi-center study suggested that the high CR rates to chemoimmunotherapy regimens such as FCR obtained in academic centers may not be reproducible when the same regimens are given in the community setting. The immunomodulatory drug lenalidomide is active in relapsed high-risk CLL, but two studies of lenalidomide in previously untreated CLL patients failed to achieve a CR and were associated with significant tumor lysis, tumor flare and hematologic toxicity. In the relapsed setting, a combination study of the bifunctional alkylator bendamustine and rituximab (BR) demonstrated a high OR rate in patients with del(11q22) and del(17p13), indicating that further studies to define's bendamustine activity are warranted in high-risk CLL. Similarly, the CDK inhibitor flavopiridol demonstrated significant clinical activity and durable remissions in heavily treated, refractory CLL patients with high-risk cytogenetic features and bulky lymphadenopathy.
The monoclonal anti-CD20 antibody ofatumumab appeared to be superior to rituximab in relapsed CLL patients with bulky nodal disease or high-risk cytogenetic features.
Ongoing studies of these agents and other novel therapeutic agents in clinical development hold forth the promise that treatment options for CLL patients will continue to expand and improve.
Maddocks KJ, Lin TS.
The Ohio State University, Division of Hematology-Oncology, 320 West 10th Avenue, Columbus, Ohio 43210, USA. lin.563@osu.edu.
ABSTRACT: Advances in the treatment of chronic lymphocytic leukemia (CLL) have improved initial overall response (OR) rates, complete response (CR) rates and progression free survival (PFS). Despite these advances, CLL remains incurable with standard therapies. Thus, there remains a need for more effective therapies in both the upfront and relapsed setting, particularly for patients with high-risk cytogenetic abnormalities such as del(11q22) and del(17p13). The 2008 American Society of Hematology (ASH) Annual Meeting featured several presentations which highlighted the ongoing clinical advances in CLL. The benefit of adding rituximab to purine analog therapy in the upfront setting was demonstrated by a large randomized study which showed that the addition of rituximab to fludarabine and cyclophosphamide (FCR) significantly improved OR, CR and PFS. The improvement in PFS directly resulted from an improved ability to eliminate minimal residual disease (MRD) in the peripheral blood, highlighting the importance of MRD eradication. However, a multi-center study suggested that the high CR rates to chemoimmunotherapy regimens such as FCR obtained in academic centers may not be reproducible when the same regimens are given in the community setting. The immunomodulatory drug lenalidomide is active in relapsed high-risk CLL, but two studies of lenalidomide in previously untreated CLL patients failed to achieve a CR and were associated with significant tumor lysis, tumor flare and hematologic toxicity. In the relapsed setting, a combination study of the bifunctional alkylator bendamustine and rituximab (BR) demonstrated a high OR rate in patients with del(11q22) and del(17p13), indicating that further studies to define's bendamustine activity are warranted in high-risk CLL. Similarly, the CDK inhibitor flavopiridol demonstrated significant clinical activity and durable remissions in heavily treated, refractory CLL patients with high-risk cytogenetic features and bulky lymphadenopathy.
The monoclonal anti-CD20 antibody ofatumumab appeared to be superior to rituximab in relapsed CLL patients with bulky nodal disease or high-risk cytogenetic features.
Ongoing studies of these agents and other novel therapeutic agents in clinical development hold forth the promise that treatment options for CLL patients will continue to expand and improve.
12/12 2009 02:02 JensH 023380 Jeg forstår desværre ikke detaljerne i rapporterne ovenfor.
Men det ser da ikke helt galt ud.
Men jeg forstår denne artikel:
http://www.telegraph.co.uk/finance/financetopics/budget/6782322/GSK-commits-500m-to-UK-after-10p-tax-rate-is-introduced-in-pre-Budget-report.html
For mig ser det ud til at GSK investerer et pænt beløb for selv at kunne producere Azerra?
Men det ser da ikke helt galt ud.
Men jeg forstår denne artikel:
http://www.telegraph.co.uk/finance/financetopics/budget/6782322/GSK-commits-500m-to-UK-after-10p-tax-rate-is-introduced-in-pre-Budget-report.html
For mig ser det ud til at GSK investerer et pænt beløb for selv at kunne producere Azerra?
Hej Jens H,
Det er en meget mærkelig meddelelse. Al produktion af Arzerra er udlagt til Lonza i Schweiz. Hvis GSK overhovedet på nogen måde var interesseret i at producere Arzerra, så ville de købe genmabs fabrik. Men såvidt jeg kan læse så kredser artiklen om en udvidelse af en fabrik i UK.
Men hvis GSK går i disse tanker så burde Genmabs fabrik kunne komme i spil. Men der er intet der tyder på det.
Det er en meget mærkelig meddelelse. Al produktion af Arzerra er udlagt til Lonza i Schweiz. Hvis GSK overhovedet på nogen måde var interesseret i at producere Arzerra, så ville de købe genmabs fabrik. Men såvidt jeg kan læse så kredser artiklen om en udvidelse af en fabrik i UK.
Men hvis GSK går i disse tanker så burde Genmabs fabrik kunne komme i spil. Men der er intet der tyder på det.
12/12 2009 10:04 JensH 023383 Hej Akademiker,
Jeg er helt enig. Det er underligt.
Men der går jo nok nogle år før GSK's nye fabrik er helt oppe i omdrejninger - og i mellemtiden skal man jo også have produceret produktet. Jeg ved ikke hvor længe aftalen med Lonza løber.
Men jeg har skrevet til journalisten for at høre hvem der har sat Azerra produktion i forbindelse med fabrikken. Jeg poster her med det samme der er et svar.
Jeg er helt enig. Det er underligt.
Men der går jo nok nogle år før GSK's nye fabrik er helt oppe i omdrejninger - og i mellemtiden skal man jo også have produceret produktet. Jeg ved ikke hvor længe aftalen med Lonza løber.
Men jeg har skrevet til journalisten for at høre hvem der har sat Azerra produktion i forbindelse med fabrikken. Jeg poster her med det samme der er et svar.
Ja jeg vil tro det er grebet ud af luften, for hvorfor trods alt bruge 500 mill pund på en state-of the art factory når de kan få genmabs state of the art for 145 mill dollar + hjælpe en partner? God ide at skrive til journalisten.
Selvfølgelig kan der være subsidier fra regeringen med i spillet og det er der, men prisforskellen er så stor at det er et snuptag for GSK og overtager Genmabs fabrik. Det bliver mere og mere speget....Er Genmab og GSK røget i totterne på hinanden?
Selvfølgelig kan der være subsidier fra regeringen med i spillet og det er der, men prisforskellen er så stor at det er et snuptag for GSK og overtager Genmabs fabrik. Det bliver mere og mere speget....Er Genmab og GSK røget i totterne på hinanden?
Der har været store forventninger til Rituxan og SGN-40 (anti CD40) i kombination imod bl.a. NHL.
Roche trækker sig fra dette partnerskab:
http://www.thestreet.com/_yahoo/story/10643771/1/roche-seattle-genetics-part-ways-on-lymphoma-drug-biobuzz.html?cm_ven=YAHOO&cm_cat=FREE&cm_ite=NA
Safety på Ocrelizumab ser ud til at kunne knække den også - mener nogle forsøg er på "hold"
http://www.fiercebiotech.com/press-releases/first-phase-iii-study-evaluating-roches-ocrelizumab-patients-rheumatoid-arthritis-mee
Roche trækker sig fra dette partnerskab:
http://www.thestreet.com/_yahoo/story/10643771/1/roche-seattle-genetics-part-ways-on-lymphoma-drug-biobuzz.html?cm_ven=YAHOO&cm_cat=FREE&cm_ite=NA
Safety på Ocrelizumab ser ud til at kunne knække den også - mener nogle forsøg er på "hold"
http://www.fiercebiotech.com/press-releases/first-phase-iii-study-evaluating-roches-ocrelizumab-patients-rheumatoid-arthritis-mee
http://www.bioworld.com/servlet/com.accumedia.web.Dispatcher?next=bioWorldHeadlines_article&forceid=53000
Denne artikel omtaler de "halted" forsøg !
Denne artikel omtaler de "halted" forsøg !
Tja. Godt spørgsmål.
Meget tyder vel på, at forholdet mellem GSK og Genmab er lidt anspændt - for nu at sige det pænt. Hr. Winkels kritiske bemærkninger om den manglende milestonebetaling (for NHL i august) var jo MEGET usædvanlig, men den manglende betaling har jo også været hele bnaggrunden for, at Genmab som alternativ måtte sætte fabrikken til salg. Uanset om det nu er berettiget eller ej, så må det set fra Genmabs side vel se sådan ud, at GSK har presset dem til det yderste på finanserne, og Genmab svarer så igen med det eneste de kan gøre, hvis de vil beholde deres andel af Arzerra. Det positive i den historie er vel så, at de åbenbart mener, at der er noget at slås om. Og hvis en af grundene til GSKs nye fabrik er et ønske om at producere Arzerra på sigt, så er det jo endnu et tegn på det samme. I givet fald er det vel også et tegn på, at de går efter at opkøbe Genmab billigt (Jyske bank). Så hele denne historie kan måske være med til at kaste lidt lys over CHjorts bemærkninger i sin nye video (i den anden tråd), at der er uhørt stærke kræfter på spil i aktien for tiden.Genmab spiller bold med de store drenge, og får tørre tæsk, FORDI Genmab har fat i bolden??? Det er ikke kønt at se på, men hvis det er et udtryk for, at alle mener, at det gælder om at være boldbesiddende, så er det vel ikke kun skidt???
Meget tyder vel på, at forholdet mellem GSK og Genmab er lidt anspændt - for nu at sige det pænt. Hr. Winkels kritiske bemærkninger om den manglende milestonebetaling (for NHL i august) var jo MEGET usædvanlig, men den manglende betaling har jo også været hele bnaggrunden for, at Genmab som alternativ måtte sætte fabrikken til salg. Uanset om det nu er berettiget eller ej, så må det set fra Genmabs side vel se sådan ud, at GSK har presset dem til det yderste på finanserne, og Genmab svarer så igen med det eneste de kan gøre, hvis de vil beholde deres andel af Arzerra. Det positive i den historie er vel så, at de åbenbart mener, at der er noget at slås om. Og hvis en af grundene til GSKs nye fabrik er et ønske om at producere Arzerra på sigt, så er det jo endnu et tegn på det samme. I givet fald er det vel også et tegn på, at de går efter at opkøbe Genmab billigt (Jyske bank). Så hele denne historie kan måske være med til at kaste lidt lys over CHjorts bemærkninger i sin nye video (i den anden tråd), at der er uhørt stærke kræfter på spil i aktien for tiden.Genmab spiller bold med de store drenge, og får tørre tæsk, FORDI Genmab har fat i bolden??? Det er ikke kønt at se på, men hvis det er et udtryk for, at alle mener, at det gælder om at være boldbesiddende, så er det vel ikke kun skidt???
For nu at blive ved potentialet så er der vist ikke tidligere nogen, der har omtalt CLL konferencen i Barcelona oktober 2009. Et af de steder, hvor CLL eksperter fra hele verden mødes.
Fra CLL Global Research Foundations hjemmeside et lille udklip, mens vi venter på bear raid.
During the Immunotherapy section, a variety of strategies were presented. The Northwestern Group (Chicago) looked at a combination of antibodies to affect an immune response. This follows upon an earlier study conducted at UT M. D. Anderson Cancer Center. Dr. Tadeusz Robak presented on the recently FDA-approved antibody ofatumumab (Arzerra). It is clear that this is a major new drug giving reason for optimism for improved response to antibody therapy.
Fra CLL Global Research Foundations hjemmeside et lille udklip, mens vi venter på bear raid.
During the Immunotherapy section, a variety of strategies were presented. The Northwestern Group (Chicago) looked at a combination of antibodies to affect an immune response. This follows upon an earlier study conducted at UT M. D. Anderson Cancer Center. Dr. Tadeusz Robak presented on the recently FDA-approved antibody ofatumumab (Arzerra). It is clear that this is a major new drug giving reason for optimism for improved response to antibody therapy.
Mit link fra forleden virkede vist ikke, så I får lige nogle konklusioner.
Det er muligt, at Arzerra aldrig slår Ritux af pinden, men der er godt nok mange rundt omkring, der tror på potentialet alligevel
http://informahealthcare.com/doi/pdf/10.1517/13543780902832679
Ofatumumab has specific characteristics that differentiate it from ritux¬imab, starting from a different binding site and binding properties to longer half-life and higher intensity of CDC [24,25]. Ofatumumab is also a fully humanized MAb with a low immunogenic potential and, so far, formation of human anti-human antibodies has not been observed in patients exposed to ofatumumab. All these features allow shorter infusions with fewer infusion-related reactions than rituximab and make ofatumumab an attractive product to be used in repetitive doses in the treatment of LPDs and AIDs.
Ofatumumab as a novel anti-CD20 MAb has shown to be safe and effective, alone or in combination, in treating patients with indolent and aggressive NHL, CLL, RA and MS, but its role is not clearly defined. Probably, ofatu¬mumab will have an important role in treating patients who cannot tolerate rituximab or have developed rituximab resis¬tance; but it is unclear how ofatumumab will compare to rituximab as a single agent or in combination with chemo¬therapy in front-line settings.
Det er muligt, at Arzerra aldrig slår Ritux af pinden, men der er godt nok mange rundt omkring, der tror på potentialet alligevel
http://informahealthcare.com/doi/pdf/10.1517/13543780902832679
Ofatumumab has specific characteristics that differentiate it from ritux¬imab, starting from a different binding site and binding properties to longer half-life and higher intensity of CDC [24,25]. Ofatumumab is also a fully humanized MAb with a low immunogenic potential and, so far, formation of human anti-human antibodies has not been observed in patients exposed to ofatumumab. All these features allow shorter infusions with fewer infusion-related reactions than rituximab and make ofatumumab an attractive product to be used in repetitive doses in the treatment of LPDs and AIDs.
Ofatumumab as a novel anti-CD20 MAb has shown to be safe and effective, alone or in combination, in treating patients with indolent and aggressive NHL, CLL, RA and MS, but its role is not clearly defined. Probably, ofatu¬mumab will have an important role in treating patients who cannot tolerate rituximab or have developed rituximab resis¬tance; but it is unclear how ofatumumab will compare to rituximab as a single agent or in combination with chemo¬therapy in front-line settings.
fandt også lige dette
Genmab Punished as Arzerra Stumbles in Pivotal Trial - Glaxo Also Affected [View article] Even a biosimilar would be an incredibly lucrative drug, and even if Glaxo had to sell Arzerra at a discount to Rituxan. But so far it looks as if Arzerra is significantly more efficacious than Rituxan. Remember, both the NHL and the CLL trials were in patients for whom Rituxan had stopped working. Those patients were very sick, and the disappointment in the refractory NHL trial says nothing about how well Arzerra will do in a front-line trial. Moreover, Rituxan has a little-discussed issue--as a chimeric mab, it causes immune responses. Arzerra, which is fully human, does not. This is particularly important in non-fatal indications like arthritis. Rituxan accounts for a significant percentage of the market caps of Roche and Biogen Idec. The selloff seems wholly disproportionate; even before it dropped 30%, I think Genmab was a bargain. I think if Genmab were listed in the US and were available to a broader range of investors it would have a market cap more like that of Vertex, which in some ways is a much shakier story. For those who have the ability to buy on the OMX, this is an excellent opportunity, and I just tripled the number of shares I own.
Genmab Punished as Arzerra Stumbles in Pivotal Trial - Glaxo Also Affected [View article] Even a biosimilar would be an incredibly lucrative drug, and even if Glaxo had to sell Arzerra at a discount to Rituxan. But so far it looks as if Arzerra is significantly more efficacious than Rituxan. Remember, both the NHL and the CLL trials were in patients for whom Rituxan had stopped working. Those patients were very sick, and the disappointment in the refractory NHL trial says nothing about how well Arzerra will do in a front-line trial. Moreover, Rituxan has a little-discussed issue--as a chimeric mab, it causes immune responses. Arzerra, which is fully human, does not. This is particularly important in non-fatal indications like arthritis. Rituxan accounts for a significant percentage of the market caps of Roche and Biogen Idec. The selloff seems wholly disproportionate; even before it dropped 30%, I think Genmab was a bargain. I think if Genmab were listed in the US and were available to a broader range of investors it would have a market cap more like that of Vertex, which in some ways is a much shakier story. For those who have the ability to buy on the OMX, this is an excellent opportunity, and I just tripled the number of shares I own.
16/12 2009 13:29 223531 Det er jo det der virkeligt får en til at ligge søvnløs om natten. At selv HVIS det bare er en konkurrent eller biosimilar, selv HVIS dens effekt kun er i paritet med Rituxian, så er det jo et enormt marked man kan konkurrere om.
Når man dertil lægger at bivirkningsprofilen er bedre etc og at Genmab nok er en biobetter. så er det altså meget svært at forstå aktiemarkedets voldsomme reaktion nedefter en godkendelse på Arzerra, hvor vi er faldet fra kurs 148....men der er jo ikke meget andet at gøre end at lade salgstallene gøre sin effekt på analytikerne.
Helt ufatteligt at de på et survival studie som EGFR nu efter udsættelser som i sagens natur kun forøger sandsynligheden for succes kan vende på tallerknen og sætte det hele til peanuts. Helt igennem utroværdigt.
Når man dertil lægger at bivirkningsprofilen er bedre etc og at Genmab nok er en biobetter. så er det altså meget svært at forstå aktiemarkedets voldsomme reaktion nedefter en godkendelse på Arzerra, hvor vi er faldet fra kurs 148....men der er jo ikke meget andet at gøre end at lade salgstallene gøre sin effekt på analytikerne.
Helt ufatteligt at de på et survival studie som EGFR nu efter udsættelser som i sagens natur kun forøger sandsynligheden for succes kan vende på tallerknen og sætte det hele til peanuts. Helt igennem utroværdigt.
