Nefarious competitors are waging a negative marketing campaign aimed primarily at the FDA. The resulting label and the non-inferior assignation are what create doubt in the product's success. At the same time astute investors see the timing for acceptance and tangible proof of success will take longer than enthusiastic amateurs expect.
The box being the paradox that there can be damages when the amount is arbitrarily chosen. This would seem to be the definition of punative.
OK I've watched the arguments and read the decision (again). But I'm not totally clear on what you're saying, save for the speculation bit.
What I see is that SC found that a type 2 agreement is operant, and therefore expectation damages *can* be applied. The problem for VC is that he already found that a lump sum is too speculative, and that specific performance is out because the lats was incomplete; missing essential terms even though economic terms were definite enough to be enforceable. Further clouding the economic terms in the LATS is evidence that there was discussion of differing economic terms after the date of the term sheet.
Now he goes back and reverses himself saying a lump sum is supported by the record by way of expert testimony and a formula he devised to apply it. And yet the economic terms of the LATS provide no means for arriving at a lump sum owing to the temporal and probabilistic characteristics of the proposition.
I think what you're saying is that since there's no clear way to come to a fair and accurate way of determining what the value of the license was in 2006 using either of the two methods available under a type 2 agreement, the court can only award reliance damages.
no. just not registered with sec. means investor must be "accredited". Also implies they trust the company enough to buy stock without a current prospectus. It does mean the acquisition is dilutive.
Good find. Explains the clinical picture and the rationale for small N.
Not Afrezza specifically. Injectables do this too. But the injectables carry much higher risk of "stacking" the insulin levels which can cause hypoglycemia. The key is tighter control of the peaks with safety.
I have observed that advertising ramps up near the end of a products life. Tamiflu is a good example
What I'm seeing in research papers is that controlling post prandial BS levels decreases the amount of basal insulin needed for control. Taken together this can produce a significant reduction in A1c. A1c is a proxy for tissue damage caused by high blood sugar. Afrezza will eventually get labeled for prediabetics and gestational diabetes IMO
No decision in the appeal. Siga has submitted opening arguments. AFAIK next is PIP rebuttal. Bankruptcy proceedings come up again in June at NY court.
Awesome control. I believe this product will eventually be used to treat metabolic syndrome. 34% of adults in the US had this condition in 2009.
Thinking of losing another 20 pounds and exercising more to get off metformin. It would be tempting to take a hit of A and eat a half gallon of ice cream, though.
Normal range for A1c levels weren't established until after a major shift from fat to simple carbohydrate began to occur in our diet. I think we will find that a good fasting BS level is closer to 50 than 100. The bs spikes also affect lipid transport such that more fatty acids accumulate in blood, raising triglycerides and LDL cholesterol.
I think there is an acceptance of high blood sugar levels as long as the mean stays in a range above normal for A1c. But A1c is just a proxy for glycation. Other tissues (besides red blood cells) are affected by high sugar levels. A1c can be maintained by lowering the baseline or reducing large excursions from the base. I think the spikes are more important because they cause the T2 disease itself, presumably by causing insulin resistance over time in persons genetically predisosed.
Not surprising. Another excerpt from the article:
As Schafer hypothesized, insulin has two classes of action: (i) excitatory (autacoid), for example stimulating glucose uptake and lipid synthesis; and (ii) inhibitory (chalone), for example inhibiting lipolysis, proteolysis, glycogenolysis, gluconeogenesis and ketogenesis. These dual actions are illustrated in Fig. 1, where insulin’s well recognized action in stimulating lipogenesis from glucose (in rat adipocytes) is illustrated.6 What perhaps is less well known is insulin’s simultaneous inhibitory action on lipolysis. It is quite clear from Fig. 1 that both these actions occur simultaneously over the same concentration range. They are both mediated through the same cell membrane receptor. These actions of insulin in vitro were discovered in the late 1950s when it was also shown that insulin stimulated glucose uptake by rat muscle. It was extrapolation of this last observation in rat muscle to explain the pathophysiology of diabetes that was erroneous. The consequence of this error was the (fallacious) concept of insulin being ‘required’ for glucose entry into cells rather than just accelerating glucose uptake. The hyperglycaemia of diabetes was interpreted as a ‘damming back’ of glucose in the blood stream as a consequence of a lack of insulin. This became established teaching and, although the concept was shown to be erroneous in the mid‐1970s, the teaching has not changed. Consequently, therapy has been based on a flawed concept.
It may well be the case that the spikes and subsequent damage are what cause derangement in glucose managent. Certainly reduction in the magnitude of sugar levels around mealtime will slow progression of disease. I believe under the right circumstances type 2 diabetes can be reversed. This except from the british journal of anesthesia explains why.
Insulin normally has a tonic inhibitory control (what Schafer termed ‘chalonic’ action) on the supply of energy substrates arising mainly from metabolism in the liver, muscle and adipose tissue. Normally insulin ensures sufficient release of appropriate substrate to allow humans to cope with the eventualities of life in a highly controlled manner. Once insulin deficiency develops this control is lost, and energy substrates are over‐produced and flood the system. The metabolic consequences result from the excess of substrates not (as is often misconceived) by a lack of energy substrate getting to the tissues.
I'm a pre-diabetic, on metformin.
I did some research. Here is my conclusion: it is important to control bs spikes. The so-called basal levels primarily inhibit gluconeogenesis, the process whereby glucose is synthesized in the liver. This mechanism provides glucose for glucose-dependent tissues while sugars are not being assimilated from food. Without insulin, blood sugar rises while fasting. But basal levels are not adequate in the face of sugar liberated during digestion of food, especially simple carbohydrates. The digestive process triggers a rapid but transient release of insulin from the pancreas that triggers uptake of glucose by tissues that can sink the excess. In some individuals up to 70 times the basal levels are secreted normally to control exogenous sugar. Excessive sugar causes glycation of protein, whereby crucial proteins are rendered inactive due to permanent binding with sugar that occurs above threshold concentrations. Afrezza closely mimics this normal response to eating, thus preventing glycation. It does so first because it becomes available via the lungs in seconds rather than tens of minutes as is the case with injection. Secondly the molecule does not require preprocessing in the liver before it can be utilized.
According to the american cancer society you are wrong:
Tobacco smoking is by far the leading cause of small cell lung cancer. Most deaths due to small cell lung cancer are caused by smoking or exposure to secondhand smoke.