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SMCI RAMSAY 2018: “Characterization of Janus kinase (JAK) activation profiles in ME/CFS subgroups”, Lombardi
This research follows on from Prof Lombardi’s and Prof Kenny De Meirleir’s (KDM) prior collaborative work on the appearance of pDCs in gut biopsies of ME patients and potential resulting inflammation.
https://www.ncbi.nlm.nih.gov/m/pubmed/23422476/?i=7&from=De Meirleir, Kenny
And their humoral immunity profiling work:
https://www.ncbi.nlm.nih.gov/m/pubmed/27981498/?i=3&from=De Meirleir, Kenny
Given that KDM is medical director of the WPI (about to be renamed from Nevada Center for Biomedical Reserch - NVCBR) this work has the potential to translate into clinical trials with JAK/STAT inhibitors. Very exciting.
https://www.ncbi.nlm.nih.gov/m/pubmed/23422476/?i=7&from=De Meirleir, Kenny
And their humoral immunity profiling work:
https://www.ncbi.nlm.nih.gov/m/pubmed/27981498/?i=3&from=De Meirleir, Kenny
Given that KDM is medical director of the WPI (about to be renamed from Nevada Center for Biomedical Reserch - NVCBR) this work has the potential to translate into clinical trials with JAK/STAT inhibitors. Very exciting.
Sasha
Senior Member (Voting Rights)
RAMSAY 2018: MEET PROF. VINCENT LOMBARDI, PHDOCTOBER 9, 2018
“Characterization of Janus kinase (JAK) activation profiles in ME/CFS subgroups”
A project summary as written by Prof. Vincent Lombardi, PhD:
Several investigators have reported that ME/CFS is characterized by a dysregulation of inflammatory cytokines; small peptides that are critical for cell-to-cell communication.
When inflammatory cytokines bind to their cognate cellular receptor, a signaling cascade is triggered that ultimately result in the activation of inflammatory response genes. It is likely that this process plays a significant role in the pathophysiology of ME/CFS, as it does with several other inflammatory disease.
Most hematopoietic cytokine receptor signaling is mediated by a family of tyrosine kinases referred to as Janus kinases (JAKs) and their downstream transcription factors, referred to as STATs (signal transducers and activators of transcription).
Several diseases that are characterized by chronic cytokine-associated inflammation such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus are being successfully treated or the subject of clinical trials with drugs that inhibit the activation of JAKs.
In that ME/CFS is also characterized by systemic inflammatory cytokine production, it is reasonable to propose that some of the same drugs that are being used or developed to treat the aforementioned inflammatory diseases, may also be efficacious in treating ME/CFS.
Therefore, the overarching goal of our study is to identify specific JAK activation profiles of distinct ME/CFS subgroups, thereby addressing the feasibility of using JAK inhibitors to treat ME/CFS.
Our study may additionally provide compelling evidence to justify conducting clinical trials to evaluate the efficacy of JAK inhibitors for the treatment of ME/CFS.
“Characterization of Janus kinase (JAK) activation profiles in ME/CFS subgroups”
A project summary as written by Prof. Vincent Lombardi, PhD:
Several investigators have reported that ME/CFS is characterized by a dysregulation of inflammatory cytokines; small peptides that are critical for cell-to-cell communication.
When inflammatory cytokines bind to their cognate cellular receptor, a signaling cascade is triggered that ultimately result in the activation of inflammatory response genes. It is likely that this process plays a significant role in the pathophysiology of ME/CFS, as it does with several other inflammatory disease.
Most hematopoietic cytokine receptor signaling is mediated by a family of tyrosine kinases referred to as Janus kinases (JAKs) and their downstream transcription factors, referred to as STATs (signal transducers and activators of transcription).
Several diseases that are characterized by chronic cytokine-associated inflammation such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus are being successfully treated or the subject of clinical trials with drugs that inhibit the activation of JAKs.
In that ME/CFS is also characterized by systemic inflammatory cytokine production, it is reasonable to propose that some of the same drugs that are being used or developed to treat the aforementioned inflammatory diseases, may also be efficacious in treating ME/CFS.
Therefore, the overarching goal of our study is to identify specific JAK activation profiles of distinct ME/CFS subgroups, thereby addressing the feasibility of using JAK inhibitors to treat ME/CFS.
Our study may additionally provide compelling evidence to justify conducting clinical trials to evaluate the efficacy of JAK inhibitors for the treatment of ME/CFS.
I've broken the text up for ease of reading. The original is here:
https://solvecfs.org/ramsay-2018-meet-prof-vincent-lombardi-phd/
@Emily Taylor - Congratulations to Solve on having funded such interesting projects!
Can I put a plea in for Solve to break up mega-paragraphs on your site where you describe the research? Many PWME have difficulty reading such large blocks of text.I think @Jonathan Edwards says nay to this (inflammation).
Snowdrop
Senior Member (Voting Rights)
I could not find any specific time frame. The profile is from October 2018 so I think not for some time to come.
Meirleir is going to do an official trial in 6 months with 3 groups (Filgotinib, another JAK1 inhibitor and placebo). Filgotinib will be first available on the market in BENELUX (Belgium, Netherlands, Luxembourg) around May 2020. Price range will be around 10.000euro/year/patient according to the CEO from Galapagos. But of course if trials are succesful hopefully refunds via local governments will be possible. Meirleir says it will bring many patients into remission but I am awaiting trial results first... I stay sceptic but optimistic. Currently there are many JAK1 inhibitors in the pipeline so there is competition which is a good thing.