Biotech Values

[biotech jim]

As to TA and chart action of OMER, I really did not know. The TA guy from which I linked that chart said to prepare for a rebound, but expect the worst. I ended up doubling my position (undersized) at $17.80. I actually think the market and biotechs in particular are a bit shaky in here.

Lots of biotechs off their highs.

As to OMER and their IgA-N trial, I think their proteinuria measures are quite good with OMS-721, but I need to see more data and try to see any eGFR improvements. Patients in the trial need to be on the best current standard of care, reasonable/stable blood pressure and on optimal renin-angiotensin system blockade.

Here are two very good articles on the current state of IgA-N treatment, and some mechanisms in the clinic. Both full articles are free at the PubMed links provided.

Am J Nephrology review here

Am J Nephrol. 2018;47 Suppl 1:43-52. doi: 10.1159/000481636. Epub 2018 May 31.
Immunoglobulin A Nephropathy: Advances in Understanding of Pathogenesis and Treatment.
Lafayette RA1, Kelepouris E2.
Author information
Abstract
BACKGROUND:
Immunoglobulin A (IgA) nephropathy is the most common form of primary glomerulonephritis and has clinical associations with a wide range of inflammatory and infectious diseases. There is a substantial variation in clinical course and outcomes, with many patients not diagnosed until they present with sequelae, which may include gross hematuria, hypertension, renal insufficiency, and/or significant proteinuria. Treatment options are currently limited and directed mainly toward control of these sequelae and have limited ability to reduce the incidence of end-stage renal disease or treat the primary IgA defect.

SUMMARY:
Growing knowledge about the pathogenesis of IgA nephropathy and research into its genetic basis are helping to elucidate the course of this widely variable disease. IgA accumulation in the kidneys is thought to be the result of a number of different pathways in a "multi-hit" process that includes an initial traumatic trigger (often infection related) and subsequent memory responses that are amplified in those with a genetic predisposition to the disease and lead to an inflammatory response in susceptible individuals. Genome-wide association studies are providing new insights into the genetic variance of this autoimmune disease and are yielding information that may address both its causes and consequences. Key Messages: New treatment approaches are urgently required for the management of patients with IgA nephropathy. Novel interventions based around its inflammatory nature and "multi-hit" pathogenesis are being investigated to potentially limit disease progression.

© 2018 S. Karger AG, Basel.

International J Nephrology and Renovascular Disease review here

Int J Nephrol Renovasc Dis. 2018 Apr 12;11:137-148. doi: 10.2147/IJNRD.S129227. eCollection 2018.
Primary IgA nephropathy: current challenges and future prospects.
Penfold RS1, Prendecki M1, McAdoo S1, Tam FW1.
Author information
Abstract
IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide, exhibiting a variable clinical and pathological course and significantly contributing to the global burden of chronic kidney disease and end-stage renal disease. Current standards of care focus on optimization of antihypertensive and antiproteinuric therapies (typically renin- angiotensin system blockade) to reduce disease progression. Much recent attention has focused on whether additional immunosuppression confers better outcomes than supportive management alone, and indeed, several trials have demonstrated renoprotective effects following the use of oral corticosteroids. However, results have been inconsistent, and perceived benefits must be balanced against risks and adverse effects associated with generalized immunosuppression, as highlighted by the high-profile STOP-IgAN and TESTING clinical trials. Recent translational research in vitro and animal models of IgAN have generated greater insight into potential therapeutic targets for this complex autoimmune disease. Deeper understanding of the roles of the mucosal immune barrier, complement activation and deposition, T-cell dependent and independent mechanisms of B cell activation, and of the deposition and downstream inflammatory signaling pathways of nephritogenic polymeric IgA1 complexes (e.g., signaling of immune receptors via spleen tyrosine kinase) has formed the rationale for the development of novel agents and clinical trials of more targeted therapies. However, translating findings into clinical practice is challenging, with many immunopathological features of IgAN specific to humans. Recent comprehensive reviews outline current understanding of mechanisms of IgAN as well as ongoing and future clinical trials; it is not our aim to replicate this here. Instead, we take a mechanistic approach to current treatment strategies, outlining advantages and limitations of each before exploring ongoing research with potential translation into future targeted therapies for this complex disease.