Home Deep Analysis Omeros: Worst Has Been Priced In, Initiating With A Buy (NASDAQ:OMER)

Omeros: Worst Has Been Priced In, Initiating With A Buy (NASDAQ:OMER)

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Omeros: Worst Has Been Priced In, Initiating With A Buy (NASDAQ:OMER)



Omeros Corporation (NASDAQ:OMER) is a commercial small-cap biotech based in the US developing several pipelines targeting complement systems. The most advanced indication is Stem-cell transplant-associated TMA (TA-TMA) that already finished pivotal phase 3, atypical hemolytic uremic syndrome (aHUS) is going throughCRLrejected

Narsoplimab MOA

Narsoplimab MOA (Company source)

The complement system has three pathways, i) classical, ii) lectin, and iii) alternative pathway. Although all three pathways lead to the activation of C3 and generation of C5 convertase leading to a downstream signal that leads to cell lysis, only the classical pathway is antibody-dependent. For the classical pathway, antigen-antibody complexes are the main activators of the pathway, and only antibody classes of IgM, IgG1, IgG2, and IgG3 (key autoantibodies that are an important component of the acquired immune response to infection) can activate the C1 (to an active version C1qrs), which is the start of the classical pathway. On the other hand, the Lectin pathway, which Narsoplimab targets, are antibody independent. Mannan-binding lectin, MBL recognizes and binds to certain carbohydrates (mannan) on the surface of some microorganisms and further activates MBL-associated serine protease (MASP-1 and MASP-2) that cleaves and activates C4 and C2, generating C3 convertase. Narsoplimab, MASP-2 inhibitor, cleaves C2 but not C4, and therefore preventing C3 convertase from forming, further inhibiting downstream effects, especially inflammation that leads to the progression of IgAN disease. Proteinuria in IgAN results from i) active inflammatory lesions and ii) sclerotic glomerular lesions with hyperfiltration and tubular damage. Narsoplimab focuses on the inflammatory lesions, although we believe it shouldn’t impact the sclerotic glomerular lesions, and this may be the reason why the drug was more effective in certain patient subtypes of patients. especially those with more advanced renal function decline. An alternative pathway is another pathway that is not antibody-dependent; it is initiated by foreign cell surface proteins such as lipopolysaccharide (endotoxins) from gram-negative bacteria, Teichoic acid from gram-positive cell walls, parasites, tumor cells, nonpathogens, etc., that leads to spontaneous hydrolysis of C3 (leading to the production of C3b). The activated C3bs are continuously generated at a low rate and always circulate the blood system, although the activated form of C3 has a very short half-life, and it gets inactivated very soon unless it binds to an appropriate surface. The terminal complement is the terminal component of the complement cascade of C5b, C6, C7, C8, and C9 that leads to the formation of membrane attack complex (MAC) that leads to cell lysis. Of note, the terminal pathway is common to all pathways. A transmembrane channel formed by MAC distributes the osmotic equilibrium of the cell, lets ions pass through the channel, and water to come into the cell, leading to cells swelling and membranes being permeable to macromolecules, which then escapes from the cell; this leads to cell lysis that kills the pathogen.

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