URI:
   DIR Return Create A Forum - Home
       ---------------------------------------------------------
       MS Speaks
  HTML https://msspeaks.createaforum.com
       ---------------------------------------------------------
       *****************************************************
   DIR Return to: OCREVUS (ocrelizumab)
       *****************************************************
       #Post#: 1493--------------------------------------------------
       (Abst.) Ocrelizumab vs. placebo, ocrelizumab vs. interferon beta
       -1a (NEJM)
       By: agate Date: December 21, 2016, 6:36 pm
       ---------------------------------------------------------
       NEJM  (December 22, 2016) contains two articles on ocrelizumab
       in PPMS--one on ocrelizumab vs. placebo, the other on
       ocrelizumab vs. interferon beta-1a:
       [quote]Ocrelizumab versus Placebo in Primary Progressive
       Multiple Sclerosis
       Xavier Montalban, M.D., Stephen L. Hauser, M.D., Ludwig Kappos,
       M.D., Douglas L. Arnold, M.D., Amit Bar-Or, M.D., Giancarlo
       Comi, M.D., Jérôme de Seze, M.D., Gavin Giovannoni, M.D.,
       Hans-Peter Hartung, M.D., Bernhard Hemmer, M.D., Fred Lublin,
       M.D., Kottil W. Rammohan, M.D., Krzysztof Selmaj, M.D., Anthony
       Traboulsee, M.D., Annette Sauter, Ph.D., Donna Masterman, M.D.,
       Paulo Fontoura, M.D., Ph.D., Shibeshih Belachew, M.D., Ph.D.,
       Hideki Garren, M.D., Ph.D., Nicole Mairon, M.D., Peter Chin,
       M.D., and Jerry S. Wolinsky, M.D., for the ORATORIO Clinical
       Investigators
       BACKGROUND
       An evolving understanding of the immunopathogenesis of multiple
       sclerosis suggests that depleting B cells could be useful for
       treatment. We studied ocrelizumab, a humanized monoclonal
       antibody that selectively depletes CD20-expressing B cells, in
       the primary progressive form of the disease.
       METHODS
       In this phase 3 trial, we randomly assigned 732 patients with
       primary progressive multiple sclerosis in a 2:1 ratio to receive
       intravenous ocrelizumab (600 mg) or placebo every 24 weeks for
       at least 120 weeks and until a prespecified number of confirmed
       disability progression events had occurred. The primary end
       point was the percentage of patients with disability progression
       confirmed at 12 weeks in a time-to-event analysis.
       B cells contribute to the pathogenesis of multiple sclerosis,
       including the primary progressive form.Although the mechanisms
       of tissue injury in multiple sclerosis are uncertain, B cells
       may influence pathogenesis through antigen presentation,6
       autoantibody production,or cytokine secretion.6 B cells are
       present in meningeal inflammation, which is characteristic of
       chronic multiple sclerosis and may cause adjacent cortical
       demyelinating and neurodegenerative pathologic features.CD20 is
       a cell-surface antigen found on pre-B cells and mature and
       memory B cells but not on the earliest B-cell precursors or on
       plasma cells.Ocrelizumab is a humanized monoclonal antibody that
       selectively depletes CD20-expressing B cells while preserving
       the capacity for B-cell reconstitution and preexisting humoral
       immunity.
       A previous phase 2–3 trial of the chimeric monoclonal anti-CD20
       antibody rituximab (OLYMPUS trial) in primary progressive
       multiple sclerosis did not meet its primary efficacy end point,
       but a subgroup analysis showed delayed progression of disability
       in younger patients (<51 years of age) with evidence of
       increased inflammatory disease activity.3 Those results provided
       the rationale and in part informed the trial design for this
       investigation of ocrelizumab in patients with primary
       progressive multiple sclerosis. Here, we report results from a
       phase 3, randomized, parallel-group, double-blind,
       placebo-controlled trial (ORATORIO) that investigated the
       efficacy and safety of ocrelizumab in patients with primary
       progressive multiple sclerosis.
       RESULTS
       The percentage of patients with 12-week confirmed disability
       progression was 32.9% with ocrelizumab versus 39.3% with placebo
       (hazard ratio, 0.76; 95% confidence interval [CI], 0.59 to 0.98;
       P=0.03). The percentage of patients with 24-week confirmed
       disability progression was 29.6% with ocrelizumab versus 35.7%
       with placebo (hazard ratio, 0.75; 95% CI, 0.58 to 0.98; P=0.04).
       By week 120, performance on the timed 25-foot walk worsened by
       38.9% with ocrelizumab versus 55.1% with placebo (P=0.04); the
       total volume of brain lesions on T2-weighted magnetic resonance
       imaging (MRI) decreased by 3.4% with ocrelizumab and increased
       by 7.4% with placebo (P<0.001); and the percentage of
       brain-volume loss was 0.90% with ocrelizumab versus 1.09% with
       placebo (P=0.02). There was no significant difference in the
       change in the Physical Component Summary score of the 36-Item
       Short-Form Health Survey.
       Infusion-related reactions, upper respiratory tract infections,
       and oral herpes infections were more frequent with ocrelizumab
       than with placebo.
       Neoplasms occurred in 2.3% of patients who received ocrelizumab
       and in 0.8% of patients who received placebo; there was no
       clinically significant difference between groups in the rates of
       serious adverse events and serious infections.
       CONCLUSIONS
       Among patients with primary progressive multiple sclerosis,
       ocrelizumab was associated with lower rates of clinical and MRI
       progression than placebo. Extended observation is required to
       determine the long-term safety and efficacy of ocrelizumab.
       (Funded by F. Hoffmann–La Roche; ORATORIO ClinicalTrials.gov
       number, NCT01194570.)[/quote]
       For discussion, see
  HTML http://www.nejm.org/doi/full/10.1056/NEJMoa1606468?query=TOC#t=articleDiscussion
  HTML http://www.nejm.org/doi/full/10.1056/NEJMoa1606468?query=TOC#t=articleDiscussion.
       The entire article can be seen here
  HTML http://www.nejm.org/doi/full/10.1056/NEJMoa1606468?query=TOC#t=articleTop.
       _________________________________________
       [quote]Ocrelizumab versus Interferon Beta-1a in Relapsing
       Multiple Sclerosis
       Stephen L. Hauser, M.D., Amit Bar-Or, M.D., Giancarlo Comi,
       M.D., Gavin Giovannoni, M.D., Hans-Peter Hartung, M.D., Bernhard
       Hemmer, M.D., Fred Lublin, M.D., Xavier Montalban, M.D., Kottil
       W. Rammohan, M.D., Krzysztof Selmaj, M.D., Anthony Traboulsee,
       M.D., Jerry S. Wolinsky, M.D., Douglas L. Arnold, M.D., Gaelle
       Klingelschmitt, Ph.D., Donna Masterman, M.D., Paulo Fontoura,
       M.D., Ph.D., Shibeshih Belachew, M.D., Ph.D., Peter Chin, M.D.,
       Nicole Mairon, M.D., Hideki Garren, M.D., Ph.D., and Ludwig
       Kappos, M.D., for the OPERA I and OPERA II Clinical
       Investigators
       BACKGROUND
       B cells influence the pathogenesis of multiple sclerosis.
       Ocrelizumab is a humanized monoclonal antibody that selectively
       depletes CD20+ B cells.
       METHODS
       In two identical phase 3 trials, we randomly assigned 821 and
       835 patients with relapsing multiple sclerosis to receive
       intravenous ocrelizumab at a dose of 600 mg every 24 weeks or
       subcutaneous interferon beta-1a at a dose of 44 &#956;g three
       times weekly for 96 weeks. The primary end point was the
       annualized relapse rate.
       RESULTS
       The annualized relapse rate was lower with ocrelizumab than with
       interferon beta-1a in trial 1 (0.16 vs. 0.29; 46% lower rate
       with ocrelizumab; P<0.001) and in trial 2 (0.16 vs. 0.29; 47%
       lower rate; P<0.001).
       In prespecified pooled analyses, the percentage of patients with
       disability progression confirmed at 12 weeks was significantly
       lower with ocrelizumab than with interferon beta-1a (9.1% vs.
       13.6%; hazard ratio, 0.60; 95% confidence interval [CI], 0.45 to
       0.81; P<0.001), as was the percentage of patients with
       disability progression confirmed at 24 weeks (6.9% vs. 10.5%;
       hazard ratio, 0.60; 95% CI, 0.43 to 0.84; P=0.003).
       The mean number of gadolinium-enhancing lesions per T1-weighted
       magnetic resonance scan was 0.02 with ocrelizumab versus 0.29
       with interferon beta-1a in trial 1 (94% lower number of lesions
       with ocrelizumab, P<0.001) and 0.02 versus 0.42 in trial 2 (95%
       lower number of lesions, P<0.001).
       The change in the Multiple Sclerosis Functional Composite score
       (a composite measure of walking speed, upper-limb movements, and
       cognition; for this z score, negative values indicate worsening
       and positive values indicate improvement) significantly favored
       ocrelizumab over interferon beta-1a in trial 2 (0.28 vs. 0.17,
       P=0.004) but not in trial 1 (0.21 vs. 0.17, P=0.33).
       Infusion-related reactions occurred in 34.3% of the patients
       treated with ocrelizumab. Serious infection occurred in 1.3% of
       the patients treated with ocrelizumab and in 2.9% of those
       treated with interferon beta-1a. Neoplasms occurred in 0.5% of
       the patients treated with ocrelizumab and in 0.2% of those
       treated with interferon beta-1a.
       CONCLUSIONS
       Among patients with relapsing multiple sclerosis, ocrelizumab
       was associated with lower rates of disease activity and
       progression than interferon beta-1a over a period of 96 weeks.
       Larger and longer studies of the safety of ocrelizumab are
       required. (Funded by F. Hoffmann–La Roche; OPERA I and II
       ClinicalTrials.gov numbers, NCT01247324 and NCT01412333,
       respectively.)[/quote]
       The entire article can be seen here
  HTML http://www.nejm.org/doi/full/10.1056/NEJMoa1601277#t=articleTop.
       #Post#: 1494--------------------------------------------------
       B-cell depletion: A frontier in monoclonal antibodies for MS
       By: agate Date: December 21, 2016, 6:45 pm
       ---------------------------------------------------------
       NEJM Editorial about these two articles (December 22, 2016) by
       Peter Calabresi, MD that gives a coherent summary of their
       results:
       [quote]EDITORIAL
       B-Cell Depletion — A Frontier in Monoclonal Antibodies for
       Multiple Sclerosis
       Peter A. Calabresi, M.D.
       Multiple sclerosis is a disabling autoimmune disease in which
       immune cells target central nervous system (CNS) antigens,
       leading to demyelination, glial activation, and subsequent loss
       of neurons and axons. There are three main subtypes of multiple
       sclerosis: relapsing–remitting, in which patients recover partly
       or fully from attacks but go on to have others; secondary
       progressive, in which patients with relapsing–remitting disease
       have progression of disability between attacks; and primary
       progressive, in which patients have continual progression from
       the time of onset of the disease.
       Over the past two decades, a remarkable number of new therapies
       have been developed that reduce the rate of relapses, reduce
       accumulation of lesions seen on magnetic resonance imaging
       (MRI), and modestly slow disability, but these are effective
       almost exclusively in relapsing multiple sclerosis.
       Most therapies for multiple sclerosis target T-cell activation,
       the trafficking of these cells into the CNS, and effector
       functions of the lymphocytes, but many have concomitant effects
       on B cells. Because B cells also migrate from the peripheral
       blood into the CNS in patients with multiple sclerosis and these
       cells produce immunoglobulins, which are a characteristic
       finding in the cerebrospinal fluid, several phase 1b and 2
       studies have tested the efficacy of the B-cell–depleting
       chimeric anti-CD20 monoclonal antibody rituximab. This therapy
       has reduced relapses and MRI activity in patients with
       relapsing–remitting multiple sclerosis but has not slowed the
       progression of disability in patients with primary progressive
       multiple sclerosis, except in a post hoc analysis of patients
       younger than 51 years of age and with gadolinium-enhancing
       lesions on MRI. Hauser et al. and Montalban et al. now report in
       the Journal the results of phase 3 trials of a new and fully
       humanized monoclonal anti-CD20 antibody, ocrelizumab, in two
       clinical trials in relapsing multiple sclerosis and one trial in
       primary progressive multiple sclerosis.
       In the identical trials involving patients with relapsing
       multiple sclerosis, called OPERA I and OPERA II, Hauser et al.
       compared ocrelizumab at a dose of 600 mg every 24 weeks versus
       interferon beta-1a at a dose of 44 &#956;g three times a week
       for 96 weeks. Both trials showed a significant effect of
       ocrelizumab on the primary outcome of annualized relapse rate,
       with ocrelizumab resulting in a 46% or 47% lower rate than with
       interferon beta-1a. The percentage of patients with disability
       progression and the number of lesions on MRI were also
       significantly lower in the ocrelizumab group. Remarkably, in the
       ORATORIO trial by Montalban et al. involving patients with
       primary progressive multiple sclerosis, a previously untreatable
       subtype of the disease, the relative risk of disability
       progression was approximately 25% lower among patients who
       received 600 mg of ocrelizumab every 24 weeks for at least 120
       weeks than among those who received placebo. In addition, the
       total volume of brain lesions on T2-weighted MRI decreased with
       ocrelizumab and increased with placebo. This is the first drug
       to show a significant effect in slowing disability progression
       in a phase 3 trial in primary progressive multiple sclerosis,
       and therefore the trial represents a landmark study in the
       field.
       The mechanism by which B-cell depletion achieves these effects
       is not fully understood but may be multifunctional, because B
       cells have important roles in antibody secretion, antigen
       presentation, and the release of effector cytokines. Although
       there are several other antigen-presenting cells, such as
       dendritic cells and monocytes, B cells by virtue of their number
       may be important antigen-presenting cells in multiple sclerosis.
       Previous studies have shown that rituximab rapidly reduced
       secretion of the inflammatory cytokines interferon-&#947; and
       interleukin-17 from T cells in patients with multiple sclerosis,
       findings that are consistent with the early reduction of active
       gadolinium-enhancing lesions observed with anti-CD20 therapy.
       In addition, the B cell is a reservoir for Epstein–Barr virus,
       which has been implicated in the pathogenesis of multiple
       sclerosis by virtue of its high sequence homology with myelin
       basic protein, and it is interesting to speculate that B-cell
       depletion may eliminate this reservoir, thereby decreasing
       autoreactivity, although this has not been proven.
       Primary progressive multiple sclerosis is characterized by
       insidious progression of disability over years with no remission
       and low MRI activity, and it is generally considered less
       inflammatory and more neurodegenerative than relapsing multiple
       sclerosis. These features are cited as explanations for the
       failure of other immunosuppressive drugs to decrease disease
       progression in primary progressive multiple sclerosis.
       One possible explanation for the positive effects of ocrelizumab
       in the ORATORIO trial is that the patient population included
       younger patients (mean age, approximately 45 years) and those
       with active MRI scans (>25% had gadolinium-enhancing lesions),
       allowing for a measurable antiinflammatory effect of ocrelizumab
       in patients who had some inflammation at an early, reversible
       stage of the disease.
       Another possible explanation is that B cells may mediate
       pathologic processes by secretion of cytokines or by deposition
       of immunoglobulins after they enter the CNS. B cells and plasma
       cells secrete antibodies that may target CNS antigens such as
       myelin, neurons, and glia, which could accelerate
       neurodegeneration or inhibit myelin repair. The continued
       separation of disability progression curves in the ORATORIO
       trial beyond 52 weeks, when antiinflammatory effects have been
       maximized, and success in the relatively noninflammatory
       disorder of primary progressive multiple sclerosis suggest that
       additional mechanisms of action may be operational, and further
       study is warranted.
       Although ocrelizumab offers promise for patients with primary
       progressive multiple sclerosis, who are desperately in need of a
       therapy, side effects must also be considered. Agents that
       target the immune system often result in some degree of immune
       suppression, potentially rendering the host susceptible to
       infections and impaired immune surveillance of new cancer cells,
       which could increase the risk of neoplasms.
       Although the dreaded complication of other drugs for multiple
       sclerosis, infection with JC virus causing progressive
       multifocal leukoencephalopathy, has not been seen with B-cell
       depletion in multiple sclerosis to date, there does appear to be
       a higher-than-normal risk of herpes reactivation and of
       neoplasms, especially breast cancer. These side effects will
       need to be studied in future trials and in phase 4 monitoring in
       the community to understand the extent of the risk. Clinicians
       are urged to carefully consider which patients might benefit the
       most from ocrelizumab and to stay vigilant with regard to
       monitoring for side effects that could be managed effectively if
       detected early.[/quote]
       #Post#: 1501--------------------------------------------------
       Re: (Abst.) Ocrelizumab vs. placebo, ocrelizumab vs. interferon 
       beta-1a (NEJM)
       By: agate Date: December 26, 2016, 6:47 pm
       ---------------------------------------------------------
       This news has been selected as one of the 10 top neurology
       stories of 2016 by MedPage Today:
       [quote]MedPage Today asked specialists in neurology around the
       country to tell us what they thought were the most important
       clinical developments in 2016. These were the five most commonly
       mentioned.
       1. Ocrelizumab for Primary Progressive MS
       Multiple sclerosis experts were hoping that a new drug that
       could treat not only relapsing MS, but also progressive disease,
       would be approved by the end of the year. That's not going to
       happen, since Genentech announced the FDA has pushed back the
       PDUFA date for ocrelizumab (Ocrevus) by 3 months as it reviews
       additional data on the company's manufacturing process.
       But hopes are high that the B-cell-targeting drug will be the
       first to win approval for progressive MS. Although there are
       several treatments for relapsing disease, no other drug has ever
       been approved to treat the more aggressive form.
       Updated findings from the OPERA and ORATORIO studies were
       presented at various meetings throughout the year, and drugmaker
       Genentech has continued to tout the 24% reduced relative risk of
       disability progression in primary progressive MS, although some
       have expressed concern that its effects in PPMS are not as
       strong as in RRMS.
       "The excitement around the first effective therapy in PPMS is
       tempered by that benefit being predominantly in patients with
       active inflammation at the start of the trial, with little
       benefit seen among those without active inflammation at the
       start of the trial," said Robert Fox, MD, of the Cleveland
       Clinic. "To me, this trial suggests that patients with
       progressive MS and active inflammation may benefit from an
       anti-inflammatory therapy, but a treatment for the gradual,
       insidious progression seen in the majority of progressive MS
       patients remains elusive."
       Jerry Wolinsky, MD, of UTHealth and Memorial Hermann in Houston,
       said that even if ocrelizumab isn't approved for PPMS, "the
       effects of the drug in relapsing forms of the disease are
       impressive, and have refocused the field into considering B
       cells as contributing more to the immunopathogenesis of the
       disease than we have in the past."[/quote]
       *****************************************************