Avid Bioservices Inc (CDMO)

[biopharm]

Is it possible that Bavi or PS targeting can significantly help "autoimmune diseases" as well?

I have a couple diabetes abstracts listed at the bottom and when I see "autoimmune" across many diseases (apart from PS targeting used to help those with solid tumors/cancer), could PS targeting be next used on many of the "autoimmune" diseases? If so.... its incomprehendable to the limits that the "PS targeting platform" could reach..... "Astronomical" comes to mind first!

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I pose this scenario...so everyone take a seat here for this... because its possible, well I think it is.

A breast cancer trial takes place and lets just say 30% had CR complete responses. Now, some follow occurs 6 months later and then another 6 months after that and something happened that is freaking out the patient as well as the doctor. It turns out that the patient goes in with breast cancer... and had an "autoimmune" disease of lets say "Psoriasis" and by the 1 year follow up the doctor takes notes of this change from the patient and after the "REAL MOA" of Bavi starts to take formation.... some start to say "Oh $hit... Dr. Thorpe, you are a genius!"

Hey... biopharm doesn't like to sit idle and be content with just solid tumors. Lets aim high and make those intermittent Big Pharma nightmares a nightly occurence! : )

Autoimmune disease
Autoimmune diseases arise from an inappropriate immune response of the body against substances and tissues normally present in the body (autoimmunity). This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney). The treatment of autoimmune diseases is typically with immunosuppression—medication that decreases the immune response. A large number of autoimmune diseases are recognised.

... the list of auto-immune diseases is quite remarkable

http://en.wikipedia.org/wiki/Autoimmune_disease

Pancreatic-Derived Factor (FAM3B), a Novel Islet Cytokine, Induces Apoptosis of Insulin-Secreting ß-Cells

Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic islet ß-cells (1,2). This destruction is a complex process characterized by cellular and humoral elements of cytotoxicity (3,4). Cytotoxic actions induce at least two morphologic consequences, apoptosis and necrosis. In apoptosis, endonucleases are activated, resulting in DNA fragmentation, nuclear and cytoplasmic condensation, membrane blebbing, and cell shrinkage. In contrast, necrosis is characterized by cellular swelling, lysis, and discharge of intracellular contents (5). In autoimmune diabetes, islet-infiltrating cells (macrophages, CD4+ T-cells, and CD8+ T-cells) are thought to damage and destroy ß-cells by producing one or more cytotoxic mediators, such as free radicals, proinflammatory cytokines, Fas ligand, perforin, and granzymes (6,7). The inflammatory cytokines interleukin-1ß, tumor necrosis factor-a, and interferon-? initiate signal pathways in ß-cells, resulting in cell death through necrosis and apoptosis (4,8,9). Recent studies have shown that apoptosis is the mechanism of pancreatic islet ß-cell death in autoimmune diabetes (10–12), and the inflammatory cytokines have been shown to induce ß-cell destruction by apoptosis (13,14). In human islet cells, cytokines were also reported to induce mainly apoptosis and not necrosis (15). However, the mechanisms causing pancreatic islet ß-cells damage in autoimmune diabetes are still not fully elucidated.

http://diabetes.diabetesjournals.org/content/52/9/2296.full
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Is type 2 diabetes a chronic inflammatory/autoimmune disease?

The classification of diabetes mellitus into 2 main types, defined as Type 1 and 2 diabetes (T1DM, T2DM) relies mostly on the requirement of insulin therapy and on the presence of detectable immunologic abnormalities. However, this distinction is far from straightforward and there is considerable overlap between these 2 types of diabetes. Islet cell autoimmunity, which is characteristic of T1DM, appears in fact to be present in up to 10-15% of subjects diagnosed clinically with T2DM. In the UK Prospective Diabetes Study (UKPDS), it was reported that in patients diagnosed with in T2DM, the presence of autoantibodies to the enzyme glutamic acid decarboxylase (GAD) and cytoplasmic islet cell antibodies (ICA) were a predictor of insulin requirement as compared with patients not carrying these autoantibodies. These results are strikingly similar to a number of prospective studies carried out in childhood diabetes. If islet cell autoimmunity is truly present in 10-15% of subjects clinically diagnosed with T2DM, up to two million Americans might have an unidentified autoimmune form of T2DM, a prevalence similar to that of recent onset childhood diabetes. In addition, we found that in a subset of T2DM patients, a pronounced activation of the acute phase response that seems to be associated with islet cell autoimmunity. These results may in part explain the defect in insulin secretion as well as insulin resistance seen in T2DM. The identification of a subgroup of individuals at risk of developing T2DM using autoantibody as well as inflammatory markers is of public health interest, not only for the correct classification of diabetes, but also because immunomodulatory therapeutic strategies could potentially be instituted sufficiently early in a large number of patients diagnosed as having T2DM and most likely delay the onset of insulin requirement and the complications related with hyperglycemia.

http://www.ncbi.nlm.nih.gov/pubmed/12059095
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