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Antibody treatment for migraines


padre
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I just heard on NPR radio, today, that there is a new treatment for migraines with a better than 50% success rate for relief of at least a few days. They are treated with antibodies! Anybody "knowed" up on this? I wonder if it was tested on clusters?

Edited by padre
Correction. Antibody was always the intended topic. "Antibiotics" was a typo and an ehomonym. Thanks to Jon 019
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https://www.ncbi.nlm.nih.gov/pubmed/29124668

https://www.ncbi.nlm.nih.gov/pubmed/28389966https://www.ncbi.nlm.nih.gov/pubmed/28389966

Fremanezumab (INN) is a humanized monoclonal antibody directed against calcitonin-related polypeptides alpha and beta.[1] It is being developed for the prevention of migraine (and cluster headache) by Teva.

It is in Phase III clinical trials as of July 2017.[2][3][4] Results of two pivotal phase 3 studies were presented in 2017.[5] Teva hopes for US FDA approval in 2018.[5]

*Wikipedia*

http://www.tevapharm.com/research_development/rd_focus/pipeline/

https://www.ncbi.nlm.nih.gov/pubmed/28644160
 

I think it's the same ? just posted something similar , was looking for more information 

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There are 4 RCTs registered in cinicaltrials.gov using mAbs (monoclonal antibodies - 3 for Fremanezumab and one for Galcanezumab) as the intervention for CH and more are likely to follow.  Three of the mAbs tested with migraine had an appetite for calcitonin gene-related peptide (CGRP) and a fourth that plugs the CGRP receptor.

IMHO... the use of mAbs is still focused on the treatment of symptoms (neurogenic inflammation and the pain caused by CGRP) and not on one of the underlying causes.  If you follow the basic antibody antigen mechanism of action where an antibody attaches to an antigen (in this case CGRP), marking it for destruction by killer cells and larger white blood cells, the cow (CGRP in this case) is already out of the barn...  To my way of thinking, this means that monoclonal antibodies that attack CGRP or block its receptors will never be fully effective as they're playing a catch-up game from the get go...

Using an objective statistical measure of efficacy called the Number Needed to Treat (NNT) to prevent one migraineur from having a sever (not complete cessation) migraine headache attack, the mAb Erenumab has an NNT of 6.  That means you need to treat 6 episodic migraineurs to prevent one episodic migraineur from having a sever attack.  In other words... Erenumab was ineffective for 5 out of 6 episodic migraineurs (83%) treated.  In reality, any NNT of 10 or less is considered "good."  See the following link for more details:

http://journals.sagepub.com/doi/abs/10.1177/0333102417732504?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

In comparison, Torpiramate and Propranolo each had NNTs of 5 in preventing one episodic migraineur from having a severe attack.  Erenumab was equally effective for chronic migraineurs with an NNT of 6.  In comparison, BOTOX had an NNT of 9 and two RCTs for Torpiramate had NNTs of 13 and 4.

We won't know the efficacy of mAbs in prevneting CH until some time in 2018 or longer.  FDA approval following phase 3 studies will still be needed so two years to market as a CH prophylactic is an optimistic guess at this point.

Moreover, as these are man-made, genetically engineered foreign antibodies with no physiological means of production from within the human genome, they will need to be replaced periodically (like monthly) in order to maintain a therapeutic serum concentration...  The cost of these mAbs is still unknown at this point...  However, I strongly suspect it will be in the same price range per month as Humira (Adalimumab)... $100 to $185 out of pocket copay ($5 if AbbVie covers the injection) to $6.600 without assistance.

For reference, vitamin D3 plus Omega-3 fish oil and the vitamin D3 cofactors has a mechanism of action that downregulates/suppresses the expression of CGRP at the genetic layer... In other words, vitamin D3 bars the barn doors to prevent the cows (CGRP) from escaping the genetic layer.  Using the above statistical method of expressing efficacy, the anti-inflammatory regimen has a raw NNT of 3 or 2 in preventing one CHer from having a CH...  Numbers count...

Take care,

V/R, Batch

.

 

Edited by Batch
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Hi...might wanna change the topic title.....antibodies...not antibiotics...

btw....I was given rituximab as part of chemotherapy (2 1/2 yrs)....the incidents of ch since are VASTLY reduced...bear in mind tho...there are some side effects and alterations in your 'condition" that they can't predict or are unwilling to disclose...I am experiencing some 2 yrs after treatment....if you go in...do so with eyes WIDE OPEN!

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I'm dyslexic at times... particularly after too much rum... When that happens... I go with the flow...  BTW I had more than my share of problems with daclizumab in an open label study at NIH...  Had I known how effective vitamin D3 can be and how bad the mAbs can be...  I would never have signed the study consent form.

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batch bro...I don't believe you need to claim the dyslexia...BUT...I would advise MORE bourbon (Makers Mark...or Wild Turkey in a pinch)) and LESS rum (yuck)...tho I still look for the rum you rhapsodized (name escapes me now...starts with a B?)......

MERRY CHRISTMAS....and MANY thanks for your tireless service to clan (clusterheads) and country.............

Best

Jon

 

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The name is Bundaberg...   a.k.a., Bundy or Bundy OP (Over Proof) a.k.a., Rocket Fuel... A delightful Demerara Rum I get from Australia.  Bundy and Coke was the drink for Americans in Australia during WW II.  I float an ounce and a half on top of a perfect Mai Tai parfait. It will knock your socks off .  Too much and you come down with amnesia...  at least that's my excuse when She who must be obeyed, points out I've done something stupid...  If things get dull, you just set it on fire...

Demerara rum was first distilled from cane molasses in Guyana on the banks of the Demerara River in 1650 when British cane growers were introduced to stills and a handsome profit from the molasses that had been dumped in the river up until then.  Five years later there were 300 sugar cane plantations, 300 sugar mills and 300 stills lining the Demerara river.  The Royal Navy got into the act in 1677 when the Admiralty approved issuing a daily ration of rum to ship's crews of all rates.  By 1880 the unique flavor of aged blended rums from the Demerara region of Guyana made it a named class of rum sold worldwide by British distillers.

One of the oldest and finest of Demerara rums is El Dorado.  A 750 cc bottle of 15 year old El Dorado Demerara rum will set you back $50 and a 25 year old El Dorado goes for $500.  Needless to say this is fine sipping rum never mixed with Coca•Cola...  So much for the story of Bundaberg rum...

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