So this compound is not losing its potency, and the problem is: why, if it's still blocking gastrin receptors, why does the pH not... well, I have a theory for that, and that is that when gastrin stimulates the ECL cells we know that it stimulates the release of histamine and also switches on the synthesis of a number of peptides, many of them related to a peptide, a big thing called chromogranin A which breaks down into an poly... pancreatic polypeptide and a number of other things. Now... so on day one, if you block the action of gastrin, you block the release of histamine, but you don't block this synthesis of... because that takes time to come on. Now, my model is that these peptides inhibit... I beg your pardon, stimulate the secretion of bicarbonate. Now, there's one man who spent his life working on bicarbonate secretion and we know that it's a regulated process. So your stomach secretes mucus, but mucus is not a good buffer, but it secretes bicarbonate, and the more acid the more bicarbonate you secrete. So if you come back, then, to day one with a proton pump inhibitor, you switch off the acid, but the bicarbonate secretion is still going on, and by day seven you should start... bicarbonate is still going on, so the bicarbonate is there to raise the pH. But if you take a gastrin antagonist it blocks on day one, but we haven't yet inhibited the bicarbonate secretion so the pH rises, but by 24 hours later, though no one's mentioned it, the bicarbonate secretion will be inhibited and then the pH won't go up, but the volume will be down. So I... I... we now know from the gastrin levels that these drugs – this drug – will be a better inhibitor of acid secretion than the H2 antagonist, I think. So that is now my passion to sell this message.
