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Cortene Peptide for MECFS? "Curative"?!

Dakota15

Senior Member
Messages
300
Location
Midwest, USA
Apologies if this was already mentioned in this thread, but I believe the Bateman Center in Salt Lake City will be trialing Cortene.

I reached out to be a part of this but unfortunately where I live is not within 1,000 ft in elevation that Salt Lake City is (which is 4,500 feet - where I live is under 1,000). I believe they told me that they are hoping to be signed off in June / July by the FDA to trial, so still some time before giving it a go. They also mentioned I would need to live in SLC for 3 months, which at this time I couldn't sign up for.

Fingers crossed for this pilot.
 

tiredowl

Senior Member
Messages
170
Location
Norway
Not sure if this has been mentioned but it's possible that reducing CRH improves the leaky gut permatability, which can cause terrible brain fog.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
CT-38 is either very similar to, or identical to the (also 38 amino acid peptide) urocortin II.

Whether a ligand is considered an agonist or antagonist depends on the (competitive) receptor binding kinetics compared to the endogenous ligands.

It is highly likely that CT-38 is a CRF2 receptor agonist. It is true that receptors can be desensitised due to too much activity/"signal" by agonists. For example, the most common reason for the 5-HT1A receptor desensitisation noted in a variety of patient groups is antidepressant use! This desensitisation can persist over time too.

Just keep in mind, this is an agonist, not an antagonist.

This is the hypothesis for the "Model-Based Therapeutic Correction of Hypothalamic-Pituitary-Adrenal Axis Dysfunction" by Amos Ben-Zvi, Suzanne D. Vernon, Gordon Broderick in 2009

http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1000273

The problem with that model is it doesn't match the reality of what has been found in ME patients so far. But it is still an interesting paper worth publishing.

I don't believe that this CT-38 trial will be successful, due to it being based on flawed science. But I still believe the trial should go ahead, least of which to show that the research community still has the capacity to do clinical trials.
 

Hopeful1976

Senior Member
Messages
345
CT-38 is either very similar to, or identical to the (also 38 amino acid peptide) urocortin II.

Whether a ligand is considered an agonist or antagonist depends on the (competitive) receptor binding kinetics compared to the endogenous ligands.

It is highly likely that CT-38 is a CRF2 receptor agonist. It is true that receptors can be desensitised due to too much activity/"signal" by agonists. For example, the most common reason for the 5-HT1A receptor desensitisation noted in a variety of patient groups is antidepressant use! This desensitisation can persist over time too.

Just keep in mind, this is an agonist, not an antagonist.

This is the hypothesis for the "Model-Based Therapeutic Correction of Hypothalamic-Pituitary-Adrenal Axis Dysfunction" by Amos Ben-Zvi, Suzanne D. Vernon, Gordon Broderick in 2009

http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1000273

The problem with that model is it doesn't match the reality of what has been found in ME patients so far. But it is still an interesting paper worth publishing.

I don't believe that this CT-38 trial will be successful, due to it being based on flawed science. But I still believe the trial should go ahead, least of which to show that the research community still has the capacity to do clinical trials.
So why would Cortene invest 2 years of work into this if it was so simple that it won't be successful at all? No disrespect to you at all, but i don't understand why?
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
So why would Cortene invest 2 years of work into this if it was so simple that it won't be successful at all? No disrespect to you at all, but i don't understand why?

Depends on what you mean by success?

At the individual level, they make money from the work that they've done and gain experience at running a clinical trial.

Also keep in mind much of the research into CT-38 was before anyone ever considered whether it would be useful in ME or not. (Some of that research involved the role of urocortin II in heart disease). This sort of momentum often leads to a wish to investigate more avenues.
 

Hopeful1976

Senior Member
Messages
345
Depends on what you mean by success?

At the individual level, they make money from the work that they've done and gain experience at running a clinical trial.

Also keep in mind much of the research into CT-38 was before anyone ever considered whether it would be useful in ME or not. (Some of that research involved the role of urocortin II in heart disease). This sort of momentum often leads to a wish to investigate more avenues.
By success I mean helping us. In some capacity. @Cort seems hopeful too.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
In what way?

The first is that the "low cortisol" assumption has both low sensitivity when it comes to identifying CFS patients. (studies have been equivocal and no study has shown it to be a strong biomarker candidate with a ROC analysis)
If many patients do not have low cortisol, then it it is probably not pathological.

But that aside, the model assumes that there is an alternative steady state of lower than normal cortisol and higher than normal glucocorticoid receptor expression (or plausibly, just GCr sensitivity). This has been tested in a variety of studies - GCr receptor expression was not found to be high in a study by Jason, another study found no difference in the density or affinity of glucocorticoid receptors and studies using dexamethasone tests have been equivocal.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
Yes, CT38 is possibly a slightly modified urocortin II protein.

I believe CT38 is in fact just a new name for Procter and Gamble's drug PG873637. See this post.

You are probably correct.

I think this paper provides more info:
"Modifications of the human urocortin 2 peptide that improve pharmacological properties."
https://www.ncbi.nlm.nih.gov/pubmed/16476507
(Procter and Gamble researchers)
 

edawg81

Senior Member
Messages
142
Location
Upstate, NY
someone is claiming that this drug has been approved already by the FDA!
I couldnt find any links on the FDA website or the company website (and the company website is just a wordpress page):

Can anyone here verify this?

H
I believe this just means approve to run a phase 2 trial, not approval to market. I’m not sure the fda has this information online or not.
 

hmnr asg

Senior Member
Messages
558
That would explain the lack of any other information on the web on this.
But the tweet said " Clinicians can now test the proposed new drug" so i thought maybe it has happened and we just didnt hear about it.
Anyways thanks for the clarification,. Even if it has made it to phase 2 its good news! (if that is indeed the case).

H
 

edawg81

Senior Member
Messages
142
Location
Upstate, NY
That would explain the lack of any other information on the web on this.
But the tweet said " Clinicians can now test the proposed new drug" so i thought maybe it has happened and we just didnt hear about it.
Anyways thanks for the clarification,. Even if it has made it to phase 2 its good news! (if that is indeed the case).

H
The phase 1 trial was not specific to MECFS, so we are in uncharted territory, i think its just an orphan drug, with litte reseach supporting its use in MECFS only a hypothesis. That said im all for trials with how devastating this disease is. Rumors are the (month long?) trial will be at BH clinic in Utah. We will need to wait for more info from Cort. If I have any information incorrect please feel free to correct it.