I've discussed IFN types before. Some interesting info here that INF-β might be better to reduce inflammation/progression.
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A recent post noted that Interferon is used for MS disease. This is the other IFN type 1, IFN-β (vs our IFN-α). I checked into why the difference. It turns out there is no really good reason we don’t use IFN-β. In fact there is a good argument that IFN-β might be a better therapy. See report here discussing some history and the IFNs.
IFN-α is PEG or Besremi. IFN-β is sold for MS as “Plegridy”. Very familiar note on pegylation from 2013:
“PLEGRIDY is a new molecular entity in which interferon beta-1a is pegylated to extend its half-life and prolong its exposure in the body, enabling study of a less frequent dosing schedule”
fiercebiotech.com/biotech/b...
Since Plegridy is approved for other use, we could theoretically try it esp if one has failed IFN-α as proposed below, but no Dr is likely to do such experiments outside trials.
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Report on IFN:
Some notes, quotes:
IFN-α recent revival: rIFN-α2 unfortunately disappeared in the dark. However, the interest in using rIFN-α2 in MPNs has been revived in recent years due to the mounting evidence from several studies within the last 5–10 years
-Several studies have shown IFN-B to possess stronger anticancer capabilities (for non- MPN cancers) than IFN α–2 (PEG, Bes)
-IFN-α has limitations re inflammation leading to non-response for some, IFN β has better anti-inflam properties: There are reasons to believe that the treatment of MPN patients with IFN- β may not only have the potential to normoregulate elevated blood cell counts, but also dampen the chronic inflammatory state that accompanies MPNs and likely contributes to clonal expansion and evolution.
-IFN- β exhibits better anti-inflammatory effects via several mechanisms: However, the much stronger binding of IFN-B to IFNAR1 (50-fold) and IFNAR2 (1000-fold) than that of IFN- α, along with the potent anti-inflammatory capacity of IFN-B, might theoretically diminish the impact of the inflammatory cytokines on IFN2AR1 degradation.
-IFN- β is used for breast cancer for good reason: Early studies in breast cancer cell lines showed IFN- β to be highly superior to IFN-a; accordingly, IFN- β was suggested for the treatment of all breast cancers.
-Combo therapies:
-Tamoxifen treatment blocked the development of JAK2V617F-induced myeloproliferative neoplasms in mice and induced apoptosis (death) of human JAK2V617F+ HSPCs in a xenograft model (usually human cells in mice)
-IFN-α alone acts on the mutation indirectly through the immune system, while: Since tamoxifen augmented the antiproliferative activity of IFN- β in vitro as well as in vivo [195], it was concluded that this combination might act directly on tumor cells rather than indirectly on the immune system. (IFN-α with tamoxifen is also a possibility)
-Another proposed combo: Combination Therapy of Tamoxifen, Retinoic Acid, and rIFN-B
-IFN-α is our best bet for now but: We can conclude that stem-cell targeted therapy with rIFN-a2 will be the cornerstone in the future treatment of MPN patients. Unfortunately, a large number of patients do not tolerate rIFN-a2 or are refractory to treatment. The novel rIFN-a2b Besremi seems to be less toxic and perhaps also more effective than treatment with Pegasys, which is the only alternative today. Therefore,we are in an urgent need of stem-cell-targeting drugs other than Besremi and Pegasys, (such as IFN- β)
-Studies of the safety and efficacy of rIFN- β in patients who are refractory or intolerant to rIFN-a2 might be highly important to determine whether rIFN- β might “rescue“ such patients…repurposing rIFN-B in the treatment of MPNs is expected to open a new horizon for MPN patients.
