I found the following link regarding concerns about using snake venom:
http://www.mndassociation.org/research/ ... venom.html
The point is that little is known of how it might work and whether it does work.
I also found that Biotherapeutics used to be called Phylomed (Florida) until they started involuntary Chapter 7 bankruptcy in 2001. I think that allows them to liquidate without having to pay much if anything to their stake holders while reorganizing as Biotherapeutics. I'm not familiar with bankruptcy rules.
Some of the questions I have are:
Why did they move to the Bahamas?
Where are their publications?
Why doesn’t their website list the doctors involved?
What I have seen is that cobra venom acts in many ways but the main way is to inhibit the acetyl choline receptor to shut down the nerve synapse signals. A victim's diaphragm muscles are the first things to go which causes a loss of breathing.
The inhibition is probably an irreversible chemical bond formation between the toxic proteins and the acetylcholine receptor, preventing the receptor from ever being used again. Once about 1/3 of the receptors in a synapse are inhibited, that neuron is no longer functional.
The peptide(s) (peptides are portions of proteins) the Biotherapeutics claims to use is probably a denatured peptide(s) from one of the venom proteins. The amino acid cysteine has a sulfur atom in it. Two cysteines can crosslink their sulfur atoms to form a permanent chemical bond called a cystine bond. (think I'm spelling that right.) So when two proteins (the venom protein and the receptor) form a cystine bond together, they are permanently attached and the receptor can no longer bind and release its normal substrate, which would be acetylcholine.
Apparently they do an ozone treatment to alter the cysteines in the peptide so that the sulfurs can no longer crosslink to each other. Thereby the venom peptide
will only bind temporarily but then come off. It has the effect of perhaps slowing the acetylcholine receptor functioning but not eliminating it. Kind of a modulation effect rather than an inhibition. The peptide would have the right shape/charge distribution for binding the receptor's binding site but the peptide can no longer form the permanent bond, and so it eventually releases from the receptor, allowing acetylcholine to bind.
This would be my guess at what is going on with the peptide therapy but I don't know if it would really work, and apparently there are no or few publications even discussing it, much less proving the effectiveness of snake venom as a treatment for MS, or other diseases.
Bottom line, I wouldn't bother with this Biotherapeutics. Too many unknowns.