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Post by rrtzmd on Dec 12, 2015 15:51:59 GMT -5
The restoration of the Phase I insulin response with AFZ promotes the following:
1. Stops glucogenesis in the liver.
2. Stores glucose as glycogen in the liver.
3. Promotes synthesis of fat (fatty acids and triglycerides) by the liver.
AFZ time to 'peak' activity is much improved over lispro and results in improved post prandial glucose excursions. Timing is everything.
Over months and years of use, AFZ should reduce insulin resistance, improve lipid profile, reduce build up of Triglycerides in the liver, and reduce export of fatty acids and triglycerides by breaking the viscous cycle of excess glucose production and excess storage of fat.
I think it would be interesting to see the lipid profiles before and after AFZ therapy.
The multibillion dollar question, as a result of replacing the phase I response with AFZ, will the myriad comorbidites of vascular disease, neuropathies, and fatty liver disease reduce over the long term
with AFZ users.  As I discussed above, afrezza does nothing different than an RAA. It can't because it is just insulin like an RAA. I also pointed out that the PD graph shows time onset and effect on glucose for the first 60 minutes is almost identical to lispro, so time to "peak activity" is substantially the same. There is currently no evidence that afrezza should have any different effect on "lipid profile, etc" than any other RAA. |
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Post by rrtzmd on Dec 12, 2015 15:35:52 GMT -5
rrtzmd ... while the trials weren't designed to highlight that, at a minimum the trials do show that dosing can be done in 4u increments with non-inferior A1c and no increased hypo... does that not show that insulin to carb ratio is less important? Do you feel that if users were forced to dose SQ RAA in 4u increments they would not either sacrifice A1c results, or have increased hypo events? "...does that not show that insulin to carb ratio is less important?" Were the subjects restricted from carb counting? If not, then the type 1s most likely simply adjusted their carb counts as they titrated the dose of afrezza they were taking. |
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Post by rrtzmd on Dec 12, 2015 15:23:35 GMT -5
let's agree to narrow the focus to type one for a moment. By memory, Matt said, he was trying to wrap his head around afrezza, because he said it works nothing like subq fast acting. He said, (by memory) Afrezza stops the blood glucose level from going high in the first place. He said, subq fast acting insulins, allow blood glucose to go high and then lowers them.
regarding type 1, and this statement: The "first phase" that is shown on your graph is in response to a large IV bolus of glucose. What happens there is that the beta cells dump all their stored insulin and that produces the huge spike reply: in type one that isn't happening. I am learning and listening: did stevil hit on it the other day when he said, "The only thing that would turn off gluconeogenesis in the liver is a high insulin to glucagon ratio. That's why insulin is needed to turn it off. But I don't know why that effect would be limited to Afrezza, if that indeed is what Matt is saying..."
Read more: mnkd.proboards.com/thread/4364/sandiego?page=22#ixzz3u6VdMzQZ
good discussion, at this moment, let's narrow it to type 1. What do you all think?
Added, "The first phase begins immediately but it doesn’t lower blood glucose, instead it temporarily stops it rising. This effect seems to be responsible for all the weird and wonderful properties of Afrezza, the first phase does not happen with previous insulins. afrezzadownunder.com/ scroll down to Afrezza units and insulin; Carb ratios. " The second phase, however, works like a small dose of injectable insulin. It lowers blood glucose, and takes longer to start working. This is the only phase of Humalog or Apidra." "Previous treatments work by flooding the body with an unnaturally high level of insulin for hours, in order to slowly lower high blood glucose levels. Afrezza stops blood glucose rising in the first place using the natural first phase signal to the liver instead. This means that for the first time much lower, more natural levels of insulin can now be used in Type 1 diabetics."
– Matt
11-17-09 interview of Al Mann: www.healthline.com/diabetesmine/the-truth-about-afresa-inhalable-insulin-a-chat-with-al-mann#1"With Afrezza, there's no complex meal titration. You take a set amount, matched to your body mass and insulin resistance, determined with your doctor. You take that same amount every time you eat a meal. Then it's not important whether you eat 50 grams of carbs or 100 grams or even zero. Afrezza essentially "turns off glucogenesis" so no glucose is secreted from the liver in reaction to food. Our trial studies are showing that patients are having no more glucose highs than normal non-diabetic people, and no more lows.""With Afrezza, there's no complex meal titration...and no more lows." Has any endo ever vetted that statement? I know of no study demonstrating that, in type 1s, afrezza requires any less assessment of carb, fat and protein intake than any other RAA. And while, in type 2s, such assessment is less important, the same "no complex meal titration" applies as well to the use of RAAs. The same applies to "not important whether you eat 50 gms...etc" -- type 2s not so important, but very important in type 1s regardless of which insulin is used. "Afrezza essentially "turns off glucogenesis" -- yes in type 1 but so do RAAs; I already discussed type 2s above. "Our trial studies are showing..." and they ultimately showed that afrezza was non-inferior to lispro. |
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Post by rrtzmd on Dec 12, 2015 15:08:36 GMT -5
I think you missed my point. The "first phase" that is shown on your graph is in response to a large IV bolus of glucose. What happens there is that the beta cells dump all their stored insulin and that produces the huge spike. That does not happen when someone is simply eating a regular diet. Food has to be digested, complex sugars have to be broken down, absorption has to take place -- this is a gradual process and, consequently, there is a gradual rise in glucose accompanied by a gradual rise in insulin -- in other words, there is no similar spike on a regular diet.
I further explained that in type 2 diabetics the liver becomes unresponsive to insulin. Insulin no longer effectively suppresses gluconeogenesis. That's why they are working on drugs that affect glucose synthesis in other ways -- e.g. the mitochondrial pyruvate carrier: Regulation of Hepatic Gluconeogenesis by the Mitochondrial Pyruvate Carrier
There are several other ideas as well. For example, from that second article I linked to in my previous post: "Moreover, hypothalamic insulin resistance (central nervous system) also impairs the ability of circulating insulin to suppress glucose production, and renal tubular glucose reabsorption capacity may be enhanced despite hyperglycemia in T2DM." That's why insulin is the drug of last call in treating type 2 DM. That's one of the reasons why Type 2s typically require large doses of insulin. But the primary effect is not on the liver but on other insulin sensitive tissues. The ultimate point is that restoring that spike is, for all practical purposes, meaningless in type 2s. let's agree to narrow the focus to type one for a moment. By memory, Matt said, he was trying to wrap his head around afrezza, because he said it works nothing like subq fast acting. He said, (by memory) Afrezza stops the blood glucose level from going high in the first place. He said, subq fast acting insulins, allow blood glucose to go high and then lowers them.
regarding type 1, and this statement: The "first phase" that is shown on your graph is in response to a large IV bolus of glucose. What happens there is that the beta cells dump all their stored insulin and that produces the huge spike reply: in type one that isn't happening. I am learning and listening: did stevil hit on it the other day when he said, "The only thing that would turn off gluconeogenesis in the liver is a high insulin to glucagon ratio. That's why insulin is needed to turn it off. But I don't know why that effect would be limited to Afrezza, if that indeed is what Matt is saying..."
Read more: mnkd.proboards.com/thread/4364/sandiego?page=22#ixzz3u6VdMzQZ
good discussion, at this moment, let's narrow it to type 1. What do you all think?
Added, "The first phase begins immediately but it doesn’t lower blood glucose, instead it temporarily stops it rising. This effect seems to be responsible for all the weird and wonderful properties of Afrezza, the first phase does not happen with previous insulins. afrezzadownunder.com/ scroll down to Afrezza units and insulin; Carb ratios. " The second phase, however, works like a small dose of injectable insulin. It lowers blood glucose, and takes longer to start working. This is the only phase of Humalog or Apidra." "Previous treatments work by flooding the body with an unnaturally high level of insulin for hours, in order to slowly lower high blood glucose levels. Afrezza stops blood glucose rising in the first place using the natural first phase signal to the liver instead. This means that for the first time much lower, more natural levels of insulin can now be used in Type 1 diabetics."
– Matt
"By memory, Matt said..." Matt may not be the most reliable of witnesses. He never mentions whether he ever discusses any of his results with his endo or what his endo thinks of his results. At one point, Matt had a series of videos where he was sequentially testing his "lung function" to demonstrate afrezza had no effect. Unfortunately, he was using a peak flow meter, a device used to assess reactive airway disease -- e.g. an asthma attack. I responded on that website and pointed out that the device was useless for assessing either FEV or pulmonary function. It appears that he has now removed those videos from the blog. In any case, this statement: "...subq fast acting insulins, allow blood glucose to go high and then lowers them." ...is simply wrong. Depending on when you take the insulin, either afrezza or other RAAs can prevent hyperglycemia. As he puts it, 'timing is everything." Whether "the only thing that would turn off gluconeogenesis in the liver is a high insulin to glucagon ratio" is relevant or not is debatable. Alpha cells also become insulin insensitive in type 2 DM, which results in higher glucagon secretion, causing a corresponding increased effect on the liver. Other factors play a role as well, but I doubt that the "ratio" itself is important in type 2s. A recent brief review article discusses glucagon's role but does not appear to attach any significance to the "ratio" of insulin to glucagon: The role of glucagon on type 2 diabetes at a glanceIn type 1s, the alpha cell function is disturbed as well -- another review: Alpha cell function in type 1 diabetesAgain, I don't attach any relevance to the "ratio" myself, and the review article doesn't appear to attach any significance to it either. Everything after "what do you think" is essentially nonsense. "Doesn’t lower blood glucose, instead it temporarily stops it rising" -- insulin doesn't "temporarily" do anything. It goes in, immediately starts having its effect, and those effects persist as long as there is enough insulin to activate receptors. "The first phase does not happen with previous insulins" -- the PD graph shows a similar glucose response to either afrezza or RAA during the first 60 minutes. All RAAs produce a spike analogous to afrezza. "The second phase, however, works like a small dose of injectable insulin" -- again, this first phase, second phase stuff is simply moot. Both afrezza and RAAs produce a massive spike in insulin concentration that decreases over time. In both cases, the insulin has its effect until it reaches an ineffective concentration. "This is the only phase of Humalog or Apidra" -- simply wrong. And this: "This means that for the first time much lower, more natural levels of insulin can now be used in Type 1 diabetics." ...borders on lunacy. There's nothing "natural" about the levels of insulin produced by afrezza and RAAs -- they both produce massive spikes. There is no evidence -- at least in the clinical literature -- that either afrezza or RAAs reduce insulin requirements. If anything, from reviewing patient reports, it appears that afrezza requires the application of significantly more insulin in order to maintain glucose control.
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Post by rrtzmd on Dec 11, 2015 21:34:45 GMT -5
Restoring the "first phase" in a type 2 doesn't matter per se. First, in real life it doesn't exist. Food is digested gradually and most sugars require one or more metabolic steps before becoming glucose. This means that invariably the rise in glucose after a meal is relatively slow. In a type 2, it really doesn't matter anyway. They are already hyperinsulinemic -- their liver is continuously bombarded with signals "to stop putting glucose into the blood." The problem is that the insulin no longer has any significant effect on liver glucose production. Indeed, scientists are working on drugs that directly affect the liver's production of glucose: Targeting glucose production in liver may lead to new diabetes therapiesNote that the article mentions one of the effects of metformin is to disrupt liver glucose production. In any case, adding more insulin won't help shut down liver glucose production. With an RAA or long acting insulin, all you're really doing is jacking up already high insulin levels and trying to overwhelm all available insulin receptors. If you're really, really interested in the subject, this is a thorough recent review on the topic: Pathogenesis of Type 2 Diabetes Mellitus
Restoring first phase insulin release absolutely matters.
Whatever the reason for the failing first phase insulin release there's an ugly feedback mechanism that kicks in when blood sugar levels rise because of that failing first phase insulin release: High levels of circulating glucose themselves are toxic to beta-cells, a phenomenon called "glucose toxicity". So as blood sugars rise these high blood sugar concentrations further damage and or kill more beta-cells, making first and second phase insulin release even less able to control blood sugar concentrations.
If your beta-cells are still able to secrete enough insulin to provide a second phase insulin release, your body may be able to bring the blood sugar back down to a normal level by 3 hours and may then go back to secreting the small amounts of basal insulin which maintain a normal or near-normal blood sugar level while you are between meals or asleep. But when first phase insulin release is weak or missing your blood sugar may easily rise over the 200 mg/dl (11 mmol/L) level currently defined as "diabetes."
At that point, two bad things happen. When the concentration of glucose in your blood reaches 200 mg/dl (11 mmol/L) your cells become insulin resistant even if they weren't insulin resistant before, so it takes a lot more insulin to lower your blood sugar from that point on.
And, even worse, the lack of a robust insulin response to the rising glucose may erroneously be interpreted by your liver as a sign that blood sugar is too low and that it is time to dump more glucose into the bloodstream. So in addition to the glucose coming in from your recent meal you also have to contend with additional glucose dumped by your poor old confused liver.
"Restoring first phase insulin release absolutely matters." No, it does not in type 2s. Please read my previous post where I try to explain that with a normal diet there is no first phase response like that shown in the graph provided by "peppy." I also explained that the "failing first phase insulin release" in type 2s occurs as a consequence of their inability to store insulin -- they are constantly secreting (because of the diabetes) and so the beta cells never accumulate enough to store, so there is no sudden dumping of of stored insulin in response to an IV bolus of glucose. That's why the second graph in the "screencast" by "peppy" is "blunted." I'm afraid your next paragraph simply makes no sense to me. Yes, there is glucose toxicity, but I'm unsure what "ugly feedback mechanism" you're referring to. The next paragraph makes sense initially, but first phase insulin release as illustrated in the graph by "peppy" has absolutely nothing to do what happens in real life. People don't routinely IV bolus large amounts of glucose at meals. From your fourth paragraph, "when the concentration of glucose in your blood reaches 200 mg/dl (11 mmol/L) your cells become insulin resistant" is simply wrong. While a number of explanations are being researched to determine what exactly causes insulin resistance, high glucose is unlikely relevant. Insulin resistance is a precursor to diabetes and, typically, it is associated with obesity. It develops gradually and the end result is elevated blood glucose as a consequence of the tissues failing to respond to insulin. Your last paragraph is a bit confusing. As I said, in type 2 diabetics, the liver becomes progressively less responsive to the effects of insulin. Type 2 diabetics are hyperinsulinemic -- they should have more than enough to suppress gluconeogenesis. However, since the liver has lost its ability to respond to insulin, yes, it continues to make glucose, but adding more insulin won't necessarily benefit suppression of that process (see my other replies above). Finally, I would add that in type 1 diabetics, there is no difference in the effect of afrezza insulin versus any other RAA on gluconeogenesis and glycogenesis. Insulin does its thing irrespective of the source. In real life, animals such as humans exhibit what is called a "cephalic phase" of digestion. In anticipation of a eating something, the hypothalamus in the brain sends signals via neurons to tell beta cells to release some insulin. This is a relatively small amount of insulin and essentially all of it is absorbed by the live. Its sole purpose is to stimulate glycogenesis and inhibit gluconeogenesis. It has nil peripheral effect. The beta cells also communicate to the alpha cells to slow down glucagon production. All this is followed by a nice, steady, gradual increase in insulin secretion in response to glucose absorption from the gut. Neither afrezza nor RAA can mimic this cephalic phase since they both involve dumping a relatively huge amount of insulin into the system where it immediately affects both the liver and the peripheral tissues. The only way to mimic the real life normal process would be some sort of pump that could introduce a small amount of insulin into the portal vein at the start of a meal followed by an insulin pump getting triggered from a glucose monitor. |
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Post by rrtzmd on Dec 11, 2015 20:52:45 GMT -5
rrtzmd
That screen cast did have the type 2 first insulin response. It was interesting.
I posted the chart because it also shows a normal non diabetic first insulin response.
Matt, a type 1, talked about a normal non diabetic first insulin response being the signaling to the liver to stop gluconeogenesis.
Matt said, he believes afrezza sends that same signal. Matt said that signal is not given with fast acting analogues.
Type 2 totally different. as you pointed out, type 2 still have working beta.
try to stay with me.
"On a side note, Matt, said, he thinks part of the affectiveness of afrezza is; Afrezza signals the first phase insulin response: which signals the liver to stop putting glucose into the blood. I kept a chart of normal first phase insulin response."
I think you missed my point. The "first phase" that is shown on your graph is in response to a large IV bolus of glucose. What happens there is that the beta cells dump all their stored insulin and that produces the huge spike. That does not happen when someone is simply eating a regular diet. Food has to be digested, complex sugars have to be broken down, absorption has to take place -- this is a gradual process and, consequently, there is a gradual rise in glucose accompanied by a gradual rise in insulin -- in other words, there is no similar spike on a regular diet. I further explained that in type 2 diabetics the liver becomes unresponsive to insulin. Insulin no longer effectively suppresses gluconeogenesis. That's why they are working on drugs that affect glucose synthesis in other ways -- e.g. the mitochondrial pyruvate carrier: Regulation of Hepatic Gluconeogenesis by the Mitochondrial Pyruvate Carrier
There are several other ideas as well. For example, from that second article I linked to in my previous post: "Moreover, hypothalamic insulin resistance (central nervous system) also impairs the ability of circulating insulin to suppress glucose production, and renal tubular glucose reabsorption capacity may be enhanced despite hyperglycemia in T2DM." That's why insulin is the drug of last call in treating type 2 DM. That's one of the reasons why Type 2s typically require large doses of insulin. But the primary effect is not on the liver but on other insulin sensitive tissues. The ultimate point is that restoring that spike is, for all practical purposes, meaningless in type 2s. |
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Post by rrtzmd on Dec 11, 2015 13:14:57 GMT -5
Agreed. Thanks for digging. I am now focused on why the difference between what the FDA considers to be the correct PD plot (Afrezza insert), vs. what Edelman presents. They are significantly different, and it could mean the difference between being considered "ultrafast" or not. Probably a non-value added discussion, but the discrepancy is bugging me. It also makes me wonder more what the PD plot from the new clamp study will look like. A better look at the charts side by side. screencast.com/t/FiCnyq01eg
more charts: screencast.com/t/VQJhkSyQrr the said duration of afrezza classified as fast acting, has always bothered me.
On a side note, Matt, said, he thinks part of the affectiveness of afrezza is; Afrezza signals the first phase insulin response: which signals the liver to stop putting glucose into the blood. I kept a chart of normal first phase insulin response. screencast.com/t/ssSzINDM his point, subq fast acting insulin does not mimic that first phase insulin response. It seems to me that information could be significant (to studies and labeling.)
You should note in your last "screencast" that they are administering an IV bolus of 20 grams of glucose. That's a lot -- about a tenth of a cup. And, being pure glucose, it has no metabolic conversion barriers that need to be overcome. Consequently, the "first phase" you see is simply the beta cells dumping their stored insulin in response to this massive slug of glucose. The "second phase" represents the beta cells recovering and synthesizing more insulin which takes longer and produces no spike. Type 2s have a "blunted" response simply because they aren't able to store any insulin. Their insulin factory can't keep up with demand as it is and, consequently, they can't store any for glucose "emergencies." Restoring the "first phase" in a type 2 doesn't matter per se. First, in real life it doesn't exist. Food is digested gradually and most sugars require one or more metabolic steps before becoming glucose. This means that invariably the rise in glucose after a meal is relatively slow. In a type 2, it really doesn't matter anyway. They are already hyperinsulinemic -- their liver is continuously bombarded with signals "to stop putting glucose into the blood." The problem is that the insulin no longer has any significant effect on liver glucose production. Indeed, scientists are working on drugs that directly affect the liver's production of glucose: Targeting glucose production in liver may lead to new diabetes therapiesNote that the article mentions one of the effects of metformin is to disrupt liver glucose production. In any case, adding more insulin won't help shut down liver glucose production. With an RAA or long acting insulin, all you're really doing is jacking up already high insulin levels and trying to overwhelm all available insulin receptors. If you're really, really interested in the subject, this is a thorough recent review on the topic: Pathogenesis of Type 2 Diabetes Mellitus |
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Post by rrtzmd on Dec 10, 2015 23:16:09 GMT -5
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Post by rrtzmd on Dec 10, 2015 23:09:11 GMT -5
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Post by rrtzmd on Dec 10, 2015 22:59:35 GMT -5
Three New Insulins Recently Added To Our List Of Options* Both approved by the FDA and now available for patients 1. U-300 glargine (Toujeo) a long acting basal insulin 2. U-100/200 degludec (Tresiba) a long acting basal insulin 3. Technosphere Inhaled insulin (Afrezza) an ultra rapid acting inhaled insulin Prandial Dosing In Type 2 Diabetes • Start with 4 to 5 units or 10% of the total basal dose, of a rapid acting analog or inhaled insulin • Add 2 units every 3 days if median BS before the next meal or bedtime (only for the pre- dinner dose) until at goal (140 to 180mg/dl) • Add 1 unit every day if the BS before the next meal or bedtime (only for the pre-dinner dose) until at goal (140 to 180 mg/dl) • Reduce the dose by 2 units if patients has hypoglycemia below 70 mg/dl tcoyd.org/PDF/2015-postp-santaclara-slides.pdfInsulin Human (Afrezza) Compared with other rapid-acting insulins: • Peaks faster and offsets faster • When added to basal insulin, equivalent A1C lowering • Lower postprandial blood glucose • Less delayed hypoglycemia Can be used in Type 1 diabetes in addition to a basal insulin (long acting insulin or basal rate via an insulin pump) Can be used in Type 2 diabetes in addition to orals alone, orals and basal, or MDI regimens Clin. Ther., 2014;Vol 36:Number 8: 1275-1289. Prandial Dosing In Type 1 Insulin to Carbohydrate Ratio Calculation: I:CHO (Type 1 and Type 2 on MDI) } Start with a ratio of 1:15 for insulin sensitive type 1 diabetics } Start with a ratio of 1:10 for insulin resistant type 2 diabetics } Formula: divide Total daily insulin dose into 500 } Example: 34 year old male with type 1 diabetes currently on 25 units of glargine (Lantus) every night and 20 to 25 units of aspart (Novolog) each day: 500/50=10 So the initial Insulin to carb ratio is 1:10 Correction Factor (CF) or Insulin Sensitivity Factor (ISP) (Type 1 andn Type 2 on MDI) Giving your patients a correction factor is a very practical tool whether they are on a pump or not The CF is an estimate of how much the BS will drop with one unit of fast acting insulin The CF usually 1:50 for insulin sensitive (<50u) patients and 1:25 for insulin resistant patients The CF can be estimated by taking the total daily insulin dose and dividing it into 1800 (the 1800 rule) You also need to pick a target glucose level for the patient (between 100 and 150) Walsh JA, Roberts R. Pumping Insulin 5th edition. 2011 Example of Determining the Correction Factor • Used at meal time AND for unexpected hyperglycemia in between meals • 21 year old female on insulin glargine 15 units at night and taking approximately 15 – 20 units a day in boluses with insulin glulisine - (1800/35 units = 51)~ CF 1:50 For those interested in details, the slides are based upon this article by Dr. Edelman: Breath of Fresh Air? A Review of Inhaled Insulin |
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Post by rrtzmd on Dec 10, 2015 14:38:28 GMT -5
This was put together by Barnstormer on StockTwits, he attended the dinner last night. Those are his comments with Dr. Edelman's comments in quotes. I'm a little confused. This StockTwits post says 150+ healthcare providers, yet the link to the TCOYD would seem to imply it is for PWD. It's at least a CME course for providers: registration page with detailsYou can also download slides from the presentation at that website. |
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Post by rrtzmd on Dec 10, 2015 11:39:51 GMT -5
The slides are here: slidesThe only thing I would note is that it appears to be a rehash of the presentation Edelman offered earlier this year in a Medscape CME course. Also, I believe most of what he says comes from a paper he wrote last year: Edelman article
A brand new article that may be of some interest: Technosphere Inhaled Insulin: Is Faster Better? |
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Post by rrtzmd on Dec 9, 2015 13:47:37 GMT -5
So is MannKind guaranteed to be screwed then or...? Afrezza could be a megablock buster if handled right by an innovative BP. It would take a few studies and some smart marketing. None of this has even been started from what I know. As for Mannkind I have no idea. Everything is a secret. We don't even know if there is a CEO (look at Matts response to an email to understand the dynamics of Mannkind), if they have cash to last 3,6,9 or 12 months, if their partner is even motivated to do anything more than the minimum (recent Sanofi deals with other diabetic companies are worrisome). The only thing I'm fairly certain about is theTS partnership vacuum. "Afrezza could be a megablock buster..." Unlikely until someone does something about that "non--inferiority" label. Unlikely until it's clear that spirometry is no longer an issue. Unlikely until diabetics are reassured that their lungs aren't at risk. Unlikely until docs are convinced afrezza is worth the extra effort. There are a lot of hurdles to overcome. I'd have to be convinced that just an "innovative BP" and "smart marketing" could get over them. |
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Post by rrtzmd on Dec 9, 2015 13:39:29 GMT -5
"I agree with all you have said, and have been pushing for the same." Pushing for the same what? How is he pushing? Who is he pushing? He always manages to say really nothing at all.
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Post by rrtzmd on Dec 9, 2015 10:31:49 GMT -5
FWIW -- another "option" for proactivity just posted on stocktwits: "Contact Sanofi IR --- they will respond" Is it possible that there is a disconnect between Afrezza awareness on boards like this, and Afrezza awareness at Sanofi? Sure, other studies are just completed or in progress through 2017, but clearly a global demand exists for Afrezza even without a formal global launch (for example, see the distribution of search sources for Afrezza on google trends). Awareness is ticking up without aggressive marketing by Sanofi, but it's their job to make the Afrezza available to patients. "...for example, see the distribution of search sources for Afrezza on google trends..." Does google trends quantify the actual number of times a topic has been searched? |
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