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Post by agedhippie on Dec 16, 2019 14:45:09 GMT -5
... Disclaimer now; it's been about four years since I looked into this so things may have moved on. The basic premise, and this is supported by the stats, is that if you have the wrong genes you have to be careful, and if you don't you can eat until you are the size of a small killer whale with no danger of ever becoming diabetic. Never mind overweight or obese, only 55% of morbidly obese people have Type 2 and if it was weight related that would be borderline impossible.Genetics certainly play a role. Age also plays a role. If anything my diet is better now than when young, but my A1c has been creeping up in past 5 years. I do totally disagree with your last clause about T2 not being weight "related". I think it clearly is, and I think even what you've said yourself is that it is. As you seem to be saying, there is ample evidence that excess fat tissue causes insulin resistance, and insulin resistance can certainly push one in the T2 direction. It was mostly the notion that this isn't true and some other cause of insulin resistance was or needed to be found. As with lots of things physiological it involves your genes as well as what you do with them. In my personal case if my A1c keeps creeping up I will try to modify behavior. I already have lower than average BMI and avoid sugar (other than holidays), but I could do better at diligence with exercise... and I suspect based on relatives that would be enough to keep me within safe range for my entire life. Some people that are overweight are quite active. I think that lowers risk quite a bit. It's the double whammy of overweight and inactive that really raises risk of diabetes... "risk" not guarantee. But in this case these "risk" factors also have clear physiological mechanisms of causality that are well understood... not simply something that has been found to correlate with the disease. Age plays a role because that deficit between the beta cells you should produce and have produced compounds with time and only matters once you hit a 40% deficit. When you are younger your deficit is lower and as you age it accumulates. Weight increases the deficit because it makes you build out beta cells to compensate for the increased insulin resistance so it does play a role if you have the genetic error. Absent that error though it has no role at all as your body happily builds the extra beta cells it needs. The other point is that the vast majority of Type 2 diabetics in Asia are not overweight. Exercise works because muscles will take up glucose directly without insulin. From memory, so I might have this reversed, muscle contractions are what does it rather than muscle stress (cardio rather than strength training at it's simplest). |
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Post by ktim on Dec 16, 2019 14:50:53 GMT -5
Was hoping someone would comment on this / what it might mean for us . I think all of the progress in closed loop pumps mean the overall market for Afrezza isn't as large as it used to be, but still ample room to have a very successful drug, way more than we've yet seen. |
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Post by agedhippie on Dec 16, 2019 14:54:52 GMT -5
And all the other small biotechs that get bought out meet that criteria? ... were bought when their product hadn't been on the market for nearly five years. BP will buy unproven sales if it believes the predictions - Sanofi did that with Mannkind. Once the sales are established then valuation becomes based on ROI and similar metrics because the data set is far more complete now and you can reduce the guess work. This is an extension of the markets buy the rumor, sell the news maxim  |
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Post by sayhey24 on Dec 16, 2019 16:21:32 GMT -5
Was hoping someone would comment on this / what it might mean for us . This is what Al was working on 20 years ago. This pump provide insulin and tries to turn off liver sugar production. If anyone could have developed the algorithms it would have been Al. But then he decided he could not overcome the fatal flaw - the lack of speed of the insulin. Afrezza obsoletes the need for this. As was seen in 118, the robust rise in insulin from afrezza blocks the alpha cells turning off sugar release by the liver. This is a great example of a Rube Goldberg now that we have afrezza. Is it interesting sure. Is it complicated, you bet. Is it needed, not with afrezza. |
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Post by shawnonafrezza on Dec 16, 2019 16:22:55 GMT -5
Was hoping someone would comment on this / what it might mean for us . This is what Al was working on 20 years ago. This pump provide insulin and tries to turn off liver sugar production. If anyone could have developed the algorithms it would have been Al. But then he decided he could not overcome the fatal flaw - the lack of speed of the insulin. Afrezza obsoletes the need for this. As was seen in 118, the robust rise in insulin from afrezza blocks the alpha cells turning off sugar release by the liver. This is a great example of a Rube Goldberg now that we have afrezza. Is it interesting sure. Is it complicated, you bet. Is it needed, not with afrezza. Yet here we are. Nobody is infallible. |
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Post by sayhey24 on Dec 16, 2019 16:43:47 GMT -5
That's not completely true. I usually stay out of Type 2 matters like this because it's not my fight, however I make an exception for the "you did it to yourself" argument. These days Type 2 is thought to be genetic with over 100 genes so far identified. The disease itself has multiple aspects depending on the Type 2 variant you are looking at, but the one thing they all have in common is insulin deficiency, not weight. The weight aspect is primarily a western issue, and in Asia the number of thin to obese Type 2 diabetics is reversed - only around 20% are obese. The current thinking is that Type 2 is due to a gap between cell death and regrowth in some people (apoptosis). This creates a deficit that accumulates with time. You become diabetic when you have an insulin deficit of around 40% (rats go down to 60% as an FYI  so that deficit may never get big enough for you to get full blown Type 2. At this point someone will ask, so why does losing weight prevent diabetes? Short answer is that it doesn't , it delays it and the ideal is that the delay is long enough for you to die of old age before it returns but that is outside your control. As you gain weight you gain insulin resistance and the body builds out beta cells so you never notice. If there is an error then you are increasing the race towards that 40% deficiency. Losing weight reduces your insulin resistance and hence the deficit pulling you away from that red line. However in the background you are still underproducing beta calls so your deficit continues to creep upwards towards that red line. The size of this error varies from person to person and thin Type 2 diabetics are thought to be more aggressive (large gap) cases. But I said this wasn't to do with weight. In some cases it is and there are genes in the identified group that act as ratchets making it easy to gain weight and very hard to lose, as well as others that push you to overeat. These are thought to be hangovers from far earlier times when the ability to gain weight was a survival trait. Type 2 is horribly complex genetically and that mess is one reason they are likely to find a cure for Type 1 before Type 2 in my opinion. Disclaimer now; it's been about four years since I looked into this so things may have moved on. The basic premise, and this is supported by the stats, is that if you have the wrong genes you have to be careful, and if you don't you can eat until you are the size of a small killer whale with no danger of ever becoming diabetic. Never mind overweight or obese, only 55% of morbidly obese people have Type 2 and if it was weight related that would be borderline impossible.Genetics certainly play a role. Age also plays a role. If anything my diet is better now than when young, but my A1c has been creeping up in past 5 years. I do totally disagree with your last clause about T2 not being weight "related". I think it clearly is, and I think even what you've said yourself is that it is. As you seem to be saying, there is ample evidence that excess fat tissue causes insulin resistance, and insulin resistance can certainly push one in the T2 direction. It was mostly the notion that this isn't true and some other cause of insulin resistance was or needed to be found. As with lots of things physiological it involves your genes as well as what you do with them. In my personal case if my A1c keeps creeping up I will try to modify behavior. I already have lower than average BMI and avoid sugar (other than holidays), but I could do better at diligence with exercise... and I suspect based on relatives that would be enough to keep me within safe range for my entire life. Some people that are overweight are quite active. I think that lowers risk quite a bit. It's the double whammy of overweight and inactive that really raises risk of diabetes... "risk" not guarantee. But in this case these "risk" factors also have clear physiological mechanisms of causality that are well understood... not simply something that has been found to correlate with the disease. Nice discussion. Now play with me and let me throw Joslin's viral theory into the mix. 1. Genetics allow certain people to fight off the virus. Then again others - the new T2s are not as lucky. In this theory the external agent is the virus. 2. Your comment about Asia is 100% correct which of course goes against the theory of fat being the root cause 3. Playing along with the virus theory and the virus can attach to the insulin receptors, what exercise and TZDs do is promoted new cell growth of cells which have yet to be corrupted by the virus. 4. Losing weight of course reduces the body's need for as much insulin therefore off loading some of the load on the pancreas but it not going to make more. Look - trying to make-up for lost insulin production by reducing weight and exercise is nobel but giving them the afrezza is a sure bet. I say do both but if you only have one option its hands down the afrezza. |
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Post by ktim on Dec 16, 2019 19:20:09 GMT -5
Genetics certainly play a role. Age also plays a role. If anything my diet is better now than when young, but my A1c has been creeping up in past 5 years. I do totally disagree with your last clause about T2 not being weight "related". I think it clearly is, and I think even what you've said yourself is that it is. As you seem to be saying, there is ample evidence that excess fat tissue causes insulin resistance, and insulin resistance can certainly push one in the T2 direction. It was mostly the notion that this isn't true and some other cause of insulin resistance was or needed to be found. As with lots of things physiological it involves your genes as well as what you do with them. In my personal case if my A1c keeps creeping up I will try to modify behavior. I already have lower than average BMI and avoid sugar (other than holidays), but I could do better at diligence with exercise... and I suspect based on relatives that would be enough to keep me within safe range for my entire life. Some people that are overweight are quite active. I think that lowers risk quite a bit. It's the double whammy of overweight and inactive that really raises risk of diabetes... "risk" not guarantee. But in this case these "risk" factors also have clear physiological mechanisms of causality that are well understood... not simply something that has been found to correlate with the disease. Nice discussion. Now play with me and let me throw Joslin's viral theory into the mix. 1. Genetics allow certain people to fight off the virus. Then again others - the new T2s are not as lucky. In this theory the external agent is the virus. 2. Your comment about Asia is 100% correct which of course goes against the theory of fat being the root cause 3. Playing along with the virus theory and the virus can attach to the insulin receptors, what exercise and TZDs do is promoted new cell growth of cells which have yet to be corrupted by the virus. 4. Losing weight of course reduces the body's need for as much insulin therefore off loading some of the load on the pancreas but it not going to make more. Look - trying to make-up for lost insulin production by reducing weight and exercise is nobel but giving them the afrezza is a sure bet. I say do both but if you only have one option its hands down the afrezza. Joslin isn't saying they think viruses cause T2, so that's your theory not theirs. Fine to have your own, just attribute it properly. Though one technical correction... the viruses do not attach to insulin receptors, it is a peptides created by the viral RNA that bind. There are likely countless viruses that have peptides that can bind to various receptors, just as plants create peptides that can interact with receptors... e.g. pot, soy, etc. In general these do not cause permanent impairment of the receptors as your theory would seem to imply you believe. In general peptides that bind to receptors are broken down and cleared from the system leaving receptors to respond to future chemical peptide signals... that's the way the system works. As for "root" cause of complicated physiological conditions, I think that is a bit of a non-scientific game of semantics. It's sort of like if someone is driving 35 mph and the brakes fail, they hit something, fly out the window and die because they aren't wearing a seat belt, is the root cause of death the brakes failing or not wearing a seat belt... or the positioning by the person that planted the tree. Root cause might be a legal concept in arguments in court about the accident, but from larger societal perspective as well as simple logical perspective there were two significant contributing factors. At this point we know conclusively that genetics, diet and exercise are significant contributing factors in T2. Only 10-15% percent of people who smoke get lung cancer though medical profession is willing to use the word "caused" in relation to lung cancers... as in 90% of all lung cancers are caused by smoking. Obviously some people have genetics that do not predispose them to be susceptible. So some, likely including the tobacco companies, might claim the root cause isn't the smoking. But looking at it from epidemiological perspective it can be shown that there is clearly a large excess number of lung cancer cases that would not have occurred if not for the smoking. Diet and exercise are very effective in reducing risk of developing T2 and in slowing its progression. Worldwide diabetes rates have been soaring and there is high correlation with adoption of "Western" diets, urbanization and more sedentary lifestyles. |
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Post by prcgorman2 on Dec 16, 2019 19:37:59 GMT -5
Hard to imagine that every BP CEO isn't fully aware of Afrezza's superior effectiveness and is keeping a close eye on the slowly increasing sales. If not the CEO directly, then their scientific advisor(s). If a BP CEO were to overlook scientific trends and only wait until they see a pre-determined level of revenue and sales growth, they would never have become a CEO. Ah yes, according to some here, MNKD has been "living in the heads of all the BP CEOs rent free" for 4 years now. That was oldie but goody trope. Wonder why that fell out of favor... maybe it was simply an introductory free rent period, and then MNKD couldn't avoid it when rent finally came due and was evicted. I've forgotten who it was that came up with that saying. Almost as catchy as "veins of gold" or "embarrassment of riches".  There has been exactly 1 other inhalable insulin on the market besides Afrezza . The executive who failed to make Exubera commercially successful at Pfizer had a similar effect on Afrezza at Sanofi when he renegged on a $1B+ worldwide marketing agreement (and as I predicted is no longer CEO of Sanofi based entirely on his record of success, or rather the lack thereof). I assume the $1B+ deal gained the attention of CEOs at Eli Lilly and Novo Nordisk.
I'm sure it felt good to make your remarks, but it can't have felt certain that no BP CEO (beside Dr. Castagna) have paid attention. I assume UTHR has a reasonable amount of notoriety and respect, and I assume their deals with MNKD have not gone completely unnoticed.
Rent free? I don't know. Veins of gold? Embarassment of riches? Not so far, but I'm not as confident those sayings won't come true as you are that MNKD goes unnoticed by BP CEOs.
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Post by ktim on Dec 16, 2019 20:18:00 GMT -5
Ah yes, according to some here, MNKD has been "living in the heads of all the BP CEOs rent free" for 4 years now. That was oldie but goody trope. Wonder why that fell out of favor... maybe it was simply an introductory free rent period, and then MNKD couldn't avoid it when rent finally came due and was evicted. I've forgotten who it was that came up with that saying. Almost as catchy as "veins of gold" or "embarrassment of riches". There has been exactly 1 other inhalable insulin on the market besides Afrezza . The executive who failed to make Exubera commercially successful at Pfizer had a similar effect on Afrezza at Sanofi when he renegged on a $1B+ worldwide marketing agreement (and as I predicted is no longer CEO of Sanofi based entirely on his record of success, or rather the lack thereof). I assume the $1B+ deal gained the attention of CEOs at Eli Lilly and Novo Nordisk.
I'm sure it felt good to make your remarks, but it can't have felt certain that no BP CEO (beside Dr. Castagna) have paid attention. I assume UTHR has a reasonable amount of notoriety and respect, and I assume their deals with MNKD have not gone completely unnoticed.
Rent free? I don't know. Veins of gold? Embarassment of riches? Not so far, but I'm not as confident those sayings won't come true as you are that MNKD goes unnoticed by BP CEOs.
Well, setting aside attempts at humor... to the extent that Afrezza got attention from higher ups at diabetes related BP (and I suspect they all took a look at it when MNKD was shopping for partner originally), they long ago would have been briefed on the technical details such as much faster pk/pd profile compared to RAA and compared to Exubera. I would imagine that with SNY dropping Afrezza they breathed a sigh of relief that it wasn't something they needed to worry about and haven't given it second thought. There is a bit of new data from very small scale trials that were somewhat "mixed" that I doubt would have materially changed anyone's views and likely not attention at CEO level. It will likely take a significant change in commercialization trajectory before any BP would take a second look at Afrezza. Obviously either view of it is speculation. I couldn't prove that there isn't one of the CEO's that has been obsessing over Afrezza, worried when it might take off but waiting to scoop up MNKD. Seems highly unlikely IMHO. More likely, at this point Afrezza isn't viewed as a threat. |
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Post by sayhey24 on Dec 16, 2019 20:33:47 GMT -5
Nice discussion. Now play with me and let me throw Joslin's viral theory into the mix. 1. Genetics allow certain people to fight off the virus. Then again others - the new T2s are not as lucky. In this theory the external agent is the virus. 2. Your comment about Asia is 100% correct which of course goes against the theory of fat being the root cause 3. Playing along with the virus theory and the virus can attach to the insulin receptors, what exercise and TZDs do is promoted new cell growth of cells which have yet to be corrupted by the virus. 4. Losing weight of course reduces the body's need for as much insulin therefore off loading some of the load on the pancreas but it not going to make more. Look - trying to make-up for lost insulin production by reducing weight and exercise is nobel but giving them the afrezza is a sure bet. I say do both but if you only have one option its hands down the afrezza. Joslin isn't saying they think viruses cause T2, so that's your theory not theirs. Fine to have your own, just attribute it properly. Though one technical correction... the viruses do not attach to insulin receptors, it is a peptides created by the viral RNA that bind. There are likely countless viruses that have peptides that can bind to various receptors, just as plants create peptides that can interact with receptors... e.g. pot, soy, etc. In general these do not cause permanent impairment of the receptors as your theory would seem to imply you believe. In general peptides that bind to receptors are broken down and cleared from the system leaving receptors to respond to future chemical peptide signals... that's the way the system works. As for "root" cause of complicated physiological conditions, I think that is a bit of a non-scientific game of semantics. It's sort of like if someone is driving 35 mph and the brakes fail, they hit something, fly out the window and die because they aren't wearing a seat belt, is the root cause of death the brakes failing or not wearing a seat belt... or the positioning by the person that planted the tree. Root cause might be a legal concept in arguments in court about the accident, but from larger societal perspective as well as simple logical perspective there were two significant contributing factors. At this point we know conclusively that genetics, diet and exercise are significant contributing factors in T2. Only 10-15% percent of people who smoke get lung cancer though medical profession is willing to use the word "caused" in relation to lung cancers... as in 90% of all lung cancers are caused by smoking. Obviously some people have genetics that do not predispose them to be susceptible. So some, likely including the tobacco companies, might claim the root cause isn't the smoking. But looking at it from epidemiological perspective it can be shown that there is clearly a large excess number of lung cancer cases that would not have occurred if not for the smoking. Diet and exercise are very effective in reducing risk of developing T2 and in slowing its progression. Worldwide diabetes rates have been soaring and there is high correlation with adoption of "Western" diets, urbanization and more sedentary lifestyles. ktim - I wish I could take credit for the virus theory but its not mine. Its actually a little more than a theory. Here is one abstract www.ncbi.nlm.nih.gov/pubmed/29467286As the abstract states its viral insulin/IGF-1-like peptides (VILPs) that binds, aka the virus or as they call it the "viral insulin". The question is after a virus has bound to a receptor does it make it harder for non-viral insulin to bind later? Something is causing new cells made through TZDs and exercise to work better than the older cells. Maybe the older ones have been corrupted by the virus - thats my theory and I will take credit for that. I could be wrong but then again I could be right. The root cause of diabetes is not up for debate. Its is simply the body is not producing enough insulin for its needs. As can be seen with the CGM nearly all T2s first lose first phase insulin release. What is up for debate is what has killed off the beta cells. As Aged said its not weight just pointing to the Asians as an example settles that. We also know genetics plays into it but why? We also know reducing the load on the pancreas allows for slowing progression and even stopping or reversing the progression. Diet and exercise are effective in reducing the risk of progression but we also know 70% progress over time. Diet and exercise probably play no role in preventing the initial destruction of the beta cells but a fit active person sure seems to have a better chance to slow or stop and maybe reverse the beta cell lose, after the fact. Then again in some they can diet and exercise until the cows come home and nothing. I have a friend who owns rehab centers and is one of the fittest people I know. His FB is now near 200 but he has not yet thrown in the towel to get the afrezza script. Pretty soon he is going to need a good meal but he has read all the web sites about dieting curing T2 diabetes. I keep telling him, its not about the diet, its about the beta cells. He is learning the hard way. Maybe another 6 month until afrezza. As I have said before why try and rely on just diet and exercise when we have the "silver bullet" in afrezza. Nearly all T2s should be started day 1 on afrezza. The same day when they are told to lose some weight and take a walk they should get the afrezza script. My advice on smoking, don't smoke. Even if you don't get cancer your fingers turn yellow and skin wrinkles up and smelling like smoke is not great. My advice is take the money you would spend on the smokes and buy MNKD stock. At least with MNKD you now have a fighting chance of not having your money go up in smoke. |
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Post by sayhey24 on Dec 16, 2019 21:00:11 GMT -5
There has been exactly 1 other inhalable insulin on the market besides Afrezza . The executive who failed to make Exubera commercially successful at Pfizer had a similar effect on Afrezza at Sanofi when he renegged on a $1B+ worldwide marketing agreement (and as I predicted is no longer CEO of Sanofi based entirely on his record of success, or rather the lack thereof). I assume the $1B+ deal gained the attention of CEOs at Eli Lilly and Novo Nordisk.
I'm sure it felt good to make your remarks, but it can't have felt certain that no BP CEO (beside Dr. Castagna) have paid attention. I assume UTHR has a reasonable amount of notoriety and respect, and I assume their deals with MNKD have not gone completely unnoticed.
Rent free? I don't know. Veins of gold? Embarassment of riches? Not so far, but I'm not as confident those sayings won't come true as you are that MNKD goes unnoticed by BP CEOs.
Well, setting aside attempts at humor... to the extent that Afrezza got attention from higher ups at diabetes related BP (and I suspect they all took a look at it when MNKD was shopping for partner originally), they long ago would have been briefed on the technical details such as much faster pk/pd profile compared to RAA and compared to Exubera. I would imagine that with SNY dropping Afrezza they breathed a sigh of relief that it wasn't something they needed to worry about and haven't given it second thought. There is a bit of new data from very small scale trials that were somewhat "mixed" that I doubt would have materially changed anyone's views and likely not attention at CEO level. It will likely take a significant change in commercialization trajectory before any BP would take a second look at Afrezza. Obviously either view of it is speculation. I couldn't prove that there isn't one of the CEO's that has been obsessing over Afrezza, worried when it might take off but waiting to scoop up MNKD. Seems highly unlikely IMHO. More likely, at this point Afrezza isn't viewed as a threat. What do you think the conversation is when the CEO says "can we make a better basal"? I think they are told "yes, but it won't be better than Tresiba" Brandicourt learned the hard way with Toujeo. What do you think the conversation is when the CEO says "Ok, if we can't do better than Tresiba, can we make a faster meal time insulin"? Do you think Paul Hudson asked those questions before he pulled the plug on Sanfoi's core business? How about the Lilly CEO when he asked "What the heck is Dave Kendall doing going to MNKD"? Novartis had a whole team camped up in Danbury for the longest time. I am pretty sure their CEO knew. Kevin Sayer who gave Onduo a boat load of DXCM stock as a buy-in said of afrezza "I have never seen anything like it". I bet most of these CEO's know who Kevin is. There use to be a video on youtube of the ADA giving the lifetime award to Al Mann. Those attending the dinner was a who's who in the diabetes community. I wish the video was still around for those who have not seen it. My advice - don't under-estimate MNKD and the power of afrezza. The question is not if. Its when and how much more dilution in the process. Everyday we get closer to connected care and insurance companies demanding T2s get connected up. As Mike said 2021 for the connected care. |
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Post by Deleted on Dec 17, 2019 1:13:26 GMT -5
Well, setting aside attempts at humor... to the extent that Afrezza got attention from higher ups at diabetes related BP (and I suspect they all took a look at it when MNKD was shopping for partner originally), they long ago would have been briefed on the technical details such as much faster pk/pd profile compared to RAA and compared to Exubera. I would imagine that with SNY dropping Afrezza they breathed a sigh of relief that it wasn't something they needed to worry about and haven't given it second thought. There is a bit of new data from very small scale trials that were somewhat "mixed" that I doubt would have materially changed anyone's views and likely not attention at CEO level. It will likely take a significant change in commercialization trajectory before any BP would take a second look at Afrezza. Obviously either view of it is speculation. I couldn't prove that there isn't one of the CEO's that has been obsessing over Afrezza, worried when it might take off but waiting to scoop up MNKD. Seems highly unlikely IMHO. More likely, at this point Afrezza isn't viewed as a threat. What do you think the conversation is when the CEO says "can we make a better basal"? I think they are told "yes, but it won't be better than Tresiba" Brandicourt learned the hard way with Toujeo. What do you think the conversation is when the CEO says "Ok, if we can't do better than Tresiba, can we make a faster meal time insulin"? Do you think Paul Hudson asked those questions before he pulled the plug on Sanfoi's core business? How about the Lilly CEO when he asked "What the heck is Dave Kendall doing going to MNKD"? Novartis had a whole team camped up in Danbury for the longest time. I am pretty sure their CEO knew. Kevin Sayer who gave Onduo a boat load of DXCM stock as a buy-in said of afrezza "I have never seen anything like it". I bet most of these CEO's know who Kevin is. There use to be a video on youtube of the ADA giving the lifetime award to Al Mann. Those attending the dinner was a who's who in the diabetes community. I wish the video was still around for those who have not seen it. My advice - don't under-estimate MNKD and the power of afrezza. The question is not if. Its when and how much more dilution in the process. Everyday we get closer to connected care and insurance companies demanding T2s get connected up. As Mike said 2021 for the connected care. The game will change when/IF Afrezza gets a better label and hopefully a new classification. Also when they get Pediatric approval in before ADA2020 it will change everything. BP will start sniffing around MNKD looking for a deal. I believe that's why Brandicourt killed the Sanofi deal. There were too many obstacles which we see now Afrezza had to overcome and if you remember Sanofi was in trouble which is why they got a new CEO. It just turned out that Brandicourt was not the answer. And we see they are killing Diabetes R&D but they could still partner with MNKD IF all comes to fruition. MNKD can improve Afrezza and Sanofi does not have to spend money. Remember when AL MANN said they are working on Afrezza 2.0? |
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Post by agedhippie on Dec 17, 2019 6:22:50 GMT -5
Was hoping someone would comment on this / what it might mean for us . This is what Al was working on 20 years ago. This pump provide insulin and tries to turn off liver sugar production. If anyone could have developed the algorithms it would have been Al. But then he decided he could not overcome the fatal flaw - the lack of speed of the insulin. Afrezza obsoletes the need for this. As was seen in 118, the robust rise in insulin from afrezza blocks the alpha cells turning off sugar release by the liver. This is a great example of a Rube Goldberg now that we have afrezza. Is it interesting sure. Is it complicated, you bet. Is it needed, not with afrezza. The job of the APS is to control the glucose level in the blood, how it does that is irrelevant and all that matters is TIR. The current generation of pumps (670G and Tandem Control-IQ) give the same results as the best that the STAT managed, the next gen due out next year increased TIR by another 10% in large scale trials. Edison was a genius, but given the choice between his bulb and an LED bulb I will take the LED bulb thank you. Al Mann tried to solve this problem back in 2000 and technology has moved on a lot since then and we see the new systems routinely out-performing Afrezza. No I am not saying this will kill Afrezza. The majority of the market will remain MDI for the same reasons that it is today - cost. |
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Post by sayhey24 on Dec 17, 2019 6:36:22 GMT -5
Al said for T1s, afrezza and the patch pump. This new pump asked about above is as I said a Rube Goldberg. Lets see what comes out of Yale with their study. We know what these guys said. www.youtube.com/watch?v=GGgGjtM5ipgAnd we know what Al said - the RAA in the AP is the fatal flaw, its too damn slow. As far as TIR when you are sleeping and only basal is on board as Al said the patch pump will do the trick. The key is reducing the complexity and that is what afrezza does. It solves the meal time complexity. Solve that and everything is so much easier. |
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Post by agedhippie on Dec 17, 2019 7:49:07 GMT -5
Al said for T1s, afrezza and the patch pump. This new pump asked about above is as I said a Rube Goldberg. Lets see what comes out of Yale with their study. We know what these guys said. www.youtube.com/watch?v=GGgGjtM5ipgAnd we know what Al said - the RAA in the AP is the fatal flaw, its too damn slow. As far as TIR when you are sleeping and only basal is on board as Al said the patch pump will do the trick. The key is reducing the complexity and that is what afrezza does. It solves the meal time complexity. Solve that and everything is so much easier. Times and technology moves on; Al's experience was from 20 years ago and his idea was never tested. In reality today you can outperform Afrezza STAT results with an off the shelf 670G and do less work to get there, and there is trial data to support those TIR claims. When the 780G is launched next year that gap gets even wider and the pump operation even simpler. And I haven't even gone near the loop systems and what they can do... |
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so that deficit may never get big enough for you to get full blown Type 2.
