Amyloid fibril formation

So I worked doing a scientific project and we were super strict, so it's why I'm saying if the test don't bring up fibril it's most likely just keeping the same standard for medication.

For example I would use the same tempture, from the same water source everyday during the scientific study we did, why? Eliminate any reasons for skewed results. Less things to blame.

They say stability, but does that mean Fibrosis happens if it's not or does it just mean they want to now it's the exact age, reconstitution, pH, tempture etc?

Like I said not saying "don't be questioning" this, it's not approved, but so far I haven't had anything say otherwise.
The linked design document talks about them testing a wide variety of formulations with different salt bridges, etc., at two different pH levels specifically because of trying to strike a balance between solubility, efficiency, and resistance to fibril formation. They have data on fibril formation at a pH of 7.5 - the study specifically looked at it. They could have chosen that as the 'standard' for the final version.

But the final patent specifies a pH of 3.5 to 4.5
 
I know not everyone is a scientist but if you are injecting this into your own body and this is a concern, you really should try to read and understand this: https://pubs.acs.org/doi/10.1021/acs.jmedchem.1c00565

maybe ask chatgpt to help explain the parts to you that you don't understand.
That doesn't sound like a good solution. The bottom-line question is whether something is safe enough to try. I wouldn't trust ChatGPT on any question involving safety.
 
I have 9 vials of 10mg cagri from QSC that I am looking to sell as well. It works for me but the fatigue I get from it is too much. Thinking about just stacking sema with reta to help with appetite suppression instead.
 
I have 9 vials of 10mg cagri from QSC that I am looking to sell as well. It works for me but the fatigue I get from it is too much. Thinking about just stacking sema with reta to help with appetite suppression instead.
stacking sema and reta is just going to give you worse results than just using reta. they are competing for the same receptor.
 
stacking sema and reta is just going to give you worse results than just using reta. they are competing for the same receptor.
According to some chart I’ve seen on this forum, Reta has very low GLP-1 activity, compared to Sema. Anecdotally people have said Reta doesn’t provide as much appetite suppression as Sema, or even Tirz. Using Sema to make up for Reta’s lower GLP-1 activity seems to make sense to me.
 
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According to some chart I’ve seen on this forum, Reta has very low GLP-1 activity, compared to Sema. Anecdotally people have said Reta doesn’t provide as much appetite suppression as Sema, or even Tirz. Using Sema to make up for Reta’s lower GLP-1 activity seems to make sense to me.
You (and many others) are making it out to be much simpler than it is. Adding in the sema just kicks the reta off the receptor and you're not using the reta to its full effect. They mix with albumin and cause completely unstudied interactions. Do whatever you want though, it's probably not dangerous but almost certainly less effective. There is a reason they picked the balance for reta that they did.
 

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