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Post by seanismorris on Nov 8, 2019 18:53:21 GMT -5
Every time I read a MannKind patent (last 5 years) I conclude:
1. Nothing new
2. Extends patent protection
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Post by mango on Dec 2, 2019 10:03:17 GMT -5
Two New MannKind Patent Applications Published 11/28/2019 1) HEAT-STABLE DRY POWDER PHARMACEUTICAL COMPOSITIONS AND METHODSAbstract:Disclosed herein are heat-stable dry powders which include peptides or protein such as oxytocin for use as a pharmaceutical composition. The composition is highly stable at increased temperatures and relatively high humid environments, and are intended for storage at room temperature with an improved shelf-life. In particular, the dry powders are intended for inhalation, however, other routes of administration can be used when reconstituted in solution. Application Date: 01.08.2019 Publication Date: 28.11.2019 Applicant:MannKind Corporation Inventors:Karine Fabio Joseph J. Guarneri Kieran Curley Marshall L. Grant Andrea Leone-Bay patentscope.wipo.int/search/en/detail.jsf?docId=US277538294&_cid=P20-K3OK0E-52675-12) MICROCRYSTALLINE DIKETOPIPERAZINE COMPOSITIONS AND METHODSAbstract:Disclosed herein are DKP microcrystals made by an improved method where they do not irreversibly self-assemble into microparticles. The microcrystals can be dispersed by atomization and re-formed by spray drying into particles having spherical shell morphology. Active agents and excipients can be incorporated into the particles by spray drying a solution containing the components to be incorporated into microcrystalline diketopiperazine particles. In particular, the microcrystalline particle compositions are suitable for pulmonary drug delivery of one or more peptides, proteins, nucleic acids and/or small organic molecules. Application Date: 06.08.2019 Publication Date: 28.11.2019 Applicant: MannKind Corporation Inventors: Bryan R. Wilson Joseph J. Guarneri Marshall L. Grant patentscope.wipo.int/search/en/detail.jsf?docId=US277539707&_cid=P20-K3OK0E-52675-1 |
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Post by mango on Dec 6, 2019 9:03:15 GMT -5
New MannKind Patent Application Published 12/5/2019 COMPOSITION AND METHOD FOR REDUCING HYPOGLYCEMIA EVENTS IN DIABETES TREATMENTAbstract: An ultra-rapid acting insulin composition and method for treating hyperglycemia in patients with diabetes are disclose. The composition is an inhalable dry powder composition comprising fumaryl diketopiperazine and insulin for pulmonary delivery, which significantly reduces the rates of hypoglycemic events in patients in patients on mealtime insulin therapy.
Type: Application
Filed: June 21, 2019
Publication date: December 5, 2019
Applicant:MannKind Corporation
Inventors: Marshall Grant, Simon R. Bruce, Robert A. Baughman
patents.justia.com/patent/20190365866patentscope.wipo.int/search/en/detail.jsf?docId=US278276878&_cid=P10-K3U7XH-21345-1—————————————————————- Snippet: Claims1. A method of treating diabetes comprising, administering to a patient with diabetes a pharmaceutical composition comprising an inhalable dry powder comprising insulin and fumaryl diketopiperazine to replace rapid acting insulin analog used at mealtime, wherein the pharmaceutical composition upon inhalation significantly reduces the rate of hypoglycemic events in the patient who is subject to severe hypoglycemia with rapid acting insulin analog treatment. |
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Post by mango on Dec 11, 2019 13:17:20 GMT -5
New MannKind Granted Patent 12/10/2019 Apparatus and method for cryogranulating a pharmaceutical compositionAbstract:Cryogranulation systems with improved dispenser assemblies are provided for use in manufacturing frozen pellets of pharmaceutical substances in a fluid medium. Methods of cryogranulating the pharmaceutical substance in the fluid medium are also provided. In particular embodiments, the dispenser assembly is used with suspensions or slurries of pharmaceutical compositions including biodegradable substances, such as proteins, peptides, and nucleic acids. In certain embodiments, the pharmaceutical substance can be adsorbed to any pharmaceutically acceptable carrier particles suitable for making pharmaceutical powders. In one embodiment, the pharmaceutical carrier can be, for example, diketopiperazine-based microparticles. The dispenser assembly improves the physical characteristics of the cryopellets formed and minimizes product loss during processing. Type: Grant Filed: August 1, 2018 Date of Patent: December 10, 2019 Assignee: MannKind Corporation Inventors: Edwin Amoro, Karel Vanackere, Michael A. White patents.justia.com/patent/10500159 |
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Post by mango on Dec 18, 2019 15:37:16 GMT -5
New One Published 12/12/2019 COMPOSITION AND METHOD FOR INHALATIONAbstract: A prostaglandin composition and method for treating pulmonary arterial hypertension is disclose. The composition is based on diketopiperazine for pulmonary inhalation. Publication Date: 12.12.2019 Applicants:MANNKIND CORPORATION Inventors:GUARNERI, Joseph J. AMIN, Nikhil GRANT, Marshall L. FREEMAN, John J. KRAFT, Kelly S. patentscope.wipo.int/search/en/detail.jsf?docId=WO2019237028&_cid=P20-K4BR5B-02328-1 |
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Post by peppy on Dec 18, 2019 19:47:05 GMT -5
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Post by peppy on Dec 19, 2019 7:52:47 GMT -5
any chance this is the undisclosed molecule? mango this was/is a European application? patentscope.wipo.int/search/en/detail.jsf;jsessionid=B310FE1C10C2975C9C517528FD7204E4.wapp1nB?docId=WO2019237028&tab=PCTDESCRIPTION[0016] Parenteral prostacyclin analogs have been the most widely studied. Intravenous epoprostenol was the first US Food and Drug Administration (FDA)-approved treatment for PAH (approved in 1995). However, due to its extremely short half-life (3-5 min), epoprostenol needs to be delivered as a continuous intravenous infusion through an indwelling catheter, with the risk of rebound PAH and acute right heart failure in case of infusion interruption. Furthermore, due to the inherent chemical instability of epoprostenol at room temperature and neutral pH (room temperature stability <8 hours), ice packs are needed to slow decomposition throughout the infusion period. A thermostable epoprostenol preparation for infusion (Veletri®), which does not require cooling, has been approved for use by the FDA. However, serious adverse events related to the delivery' system include pump malfunction, local site infection, catheter obstruction, and sepsis continues to be a barrier for its use. [0017] Treprostinil, is a longer-acting tricyclic benzidine analogue of epoprostenol with a terminal elimination half-life of approximately 2 to 4 hours and a distribution half-life of approximately 40 minutes. Unlike epoprostenol, Treprostinil is chemically stable at room temperature allowing it to be administered at ambient temperature and overcomes some of the limitations associated with epoprostenol therapy. Treprostinil causes vasodilation of pulmonary and systemic arterial vascular beds, and inhibits platelet aggregation by binding to prostacyclin IP receptors located on the surface of vascular smooth muscle cells and platelets. Treprostinil (Remodulin®) was first approved by the FDA in 2002 for adults with WHO group 1 PAH and functional class II to class IV status for continuous subcutaneous infusion and is marketed by United Therapeutics (Silver Spring, MD). In a pivotal 12 week randomized, controlled trial of 470 patients, subcutaneous Treprostinil significantly improved exercise capacity compared with placebo. The most common adverse events noted in subcutaneous infusion of Treprostinil-treated patients were infusion site pain. [0018] Currently, an oral, extended release tablet of treprostinil diolamine (Orenitran®) is also available. However, with orally delivered medications, the absorption of treprostinil may be inconsistent particularly taken with food. The pharmacological and physiochemical properties of treprostinil make this drug amenable to intermittent administration via the inhaled route. Tyvaso® and Iloprost (Ventavis®) are solutions for inhalation, which need to be administered using a special nebulizer for a prolonged period of time and often times in a physician’s office. Using Tyvaso® inhalation system [Opti- Neb ultrasonic nebulizer (NebuTec, Elsenfeld, Germany)]. The inhalation system is complex to assemble and use, cumbersome to administer the dose (patient need to reset the device 3 times during a treatment session after every 3 breaths) and was found to have high error rates in human factor study. There is a distinct risk of under dosing as patient need to take 9 breaths within a specified 90 second time limit. Additionally, breath counter mechanism is triggered by time (time related) and not by inspiration or expiration flow or effort (breath related) and thus patient can overdose or under dose themselves by taking more or less than prescribed breaths (dose) in the 90 seconds time limit. The system also requires 4 different cleaning schedule (daily, weekly, monthly and yearly). Accordingly, new methods of PAH treatment are needed to facilitate the administration of these products to a patient. [0019] Drug delivery to lung tissue has been achieved using a variety of devices for inhalation, including, nebulizers and inhalers, such as metered dose inhalers and dry powder inhalers to treat local disease or disorders. Dry powder inhalers used to deliver medicaments to the lungs contain a dose system of a powder formulation usually either in bulk supply or quantified into individual doses stored in unit dose compartments such as hard gelatin capsules or blister packs. Bulk containers are equipped with a measuring system operated by the patient in order to isolate a single dose from the powder immediately before inhalation. [0020] Dosing reproducibility with inhalers requires that the drug formulation is uniform and that the dose be delivered to a subject with consistency and reproducible results. Therefore, the dosing system ideally should operate to completely discharge all of the formulation effectively during an inspiratory maneuv |
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Post by mango on Dec 19, 2019 13:17:37 GMT -5
Based on my own research, prostaglandins are essentially Endocannabinoid-like compounds. Anandamide and prostaglandins. Re: the acids Arachidonic acid, however, also serve essential functions, particularly in cellular signalling via its precursor role for numerous oxygenated derivatives such as prostaglandins, leukotrienes, hepoxilins and other eicosanoids. Furthermore, arachidonic acid is also a structural part of endocannabinoids that have signalling functions in relation to modulation of neurotransmitter release, which might involve physiological and pathophysiological phenomena such as regulation of appetite, energy metabolism, pain perception, memory and learning. onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2826.2008.01687.x |
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Post by peppy on Dec 19, 2019 13:51:21 GMT -5
Abstract Prostaglandins are lipid autacoids derived from arachidonic acid. They both sustain homeostatic functions and mediate pathogenic mechanisms, including the inflammatory response. They are generated from arachidonate by the action of cyclooxygenase (COX) isoenzymes and their biosynthesis is blocked by nonsteroidal anti-inflammatory drugs (NSAIDs), including those selective for inhibition of COX-2. Despite the clinical efficacy of NSAIDs, prostaglandins may function in both the promotion and resolution of inflammation. This review summarizes insights into the mechanisms of prostaglandin generation and the roles of individual mediators and their receptors in modulating the inflammatory response. Prostaglandin biology has potential clinical relevance for atherosclerosis, the response to vascular injury and aortic aneurysm. Inflammation is the immune system’s response to infection and injury and has been implicated in the pathogeneses of arthritis, cancer and stroke, as well as in neurodegenerative and cardiovascular disease. Inflammation is an intrinsically beneficial event that leads to removal of offending factors and restoration of tissue structure and physiological function. The acute phase of inflammation is characterized by the rapid influx of blood granulocytes, typically neutrophils, followed swiftly by monocytes that mature into inflammatory macrophages that subsequently proliferate and thereby affect the functions of resident tissue macrophages. This process causes the cardinal signs of acute inflammation: rubor (redness), calor (heat), tumor (swelling) and dolor (pain). Once the initiating noxious stimulus is removed via phagocytosis, the inflammatory reaction can decrease and resolve. During the resolution of inflammation, granulocytes are eliminated and macrophages and lymphocytes return to normal pre-inflammatory numbers and phenotypes. The usual outcome of the acute inflammatory program is successful resolution and repair of tissue damage, rather than persistence and dysfunction of the inflammatory response, which can lead to scarring and loss of organ function. It may be anticipated, therefore, that failure of acute inflammation to resolve may predispose to auto-immunity, chronic dysplastic inflammation and excessive tissue damage (1). Prostaglandins play a key role in the generation of the inflammatory response. mangoseriously this is the undisclosed. what was the document? www.ncbi.nlm.nih.gov/pmc/articles/PMC3081099/ |
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Post by mango on Dec 19, 2019 14:37:23 GMT -5
Abstract Prostaglandins are lipid autacoids derived from arachidonic acid. They both sustain homeostatic functions and mediate pathogenic mechanisms, including the inflammatory response. They are generated from arachidonate by the action of cyclooxygenase (COX) isoenzymes and their biosynthesis is blocked by nonsteroidal anti-inflammatory drugs (NSAIDs), including those selective for inhibition of COX-2. Despite the clinical efficacy of NSAIDs, prostaglandins may function in both the promotion and resolution of inflammation. This review summarizes insights into the mechanisms of prostaglandin generation and the roles of individual mediators and their receptors in modulating the inflammatory response. Prostaglandin biology has potential clinical relevance for atherosclerosis, the response to vascular injury and aortic aneurysm. Inflammation is the immune system’s response to infection and injury and has been implicated in the pathogeneses of arthritis, cancer and stroke, as well as in neurodegenerative and cardiovascular disease. Inflammation is an intrinsically beneficial event that leads to removal of offending factors and restoration of tissue structure and physiological function. The acute phase of inflammation is characterized by the rapid influx of blood granulocytes, typically neutrophils, followed swiftly by monocytes that mature into inflammatory macrophages that subsequently proliferate and thereby affect the functions of resident tissue macrophages. This process causes the cardinal signs of acute inflammation: rubor (redness), calor (heat), tumor (swelling) and dolor (pain). Once the initiating noxious stimulus is removed via phagocytosis, the inflammatory reaction can decrease and resolve. During the resolution of inflammation, granulocytes are eliminated and macrophages and lymphocytes return to normal pre-inflammatory numbers and phenotypes. The usual outcome of the acute inflammatory program is successful resolution and repair of tissue damage, rather than persistence and dysfunction of the inflammatory response, which can lead to scarring and loss of organ function. It may be anticipated, therefore, that failure of acute inflammation to resolve may predispose to auto-immunity, chronic dysplastic inflammation and excessive tissue damage (1). Prostaglandins play a key role in the generation of the inflammatory response. mangoseriously this is the undisclosed. what was the document? www.ncbi.nlm.nih.gov/pmc/articles/PMC3081099/They already have one of these, Treprostinil, what would the other one be? What are you thinking it may be and indicated for? |
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Post by peppy on Dec 19, 2019 16:24:21 GMT -5
Abstract Prostaglandins are lipid autacoids derived from arachidonic acid. They both sustain homeostatic functions and mediate pathogenic mechanisms, including the inflammatory response. They are generated from arachidonate by the action of cyclooxygenase (COX) isoenzymes and their biosynthesis is blocked by nonsteroidal anti-inflammatory drugs (NSAIDs), including those selective for inhibition of COX-2. Despite the clinical efficacy of NSAIDs, prostaglandins may function in both the promotion and resolution of inflammation. This review summarizes insights into the mechanisms of prostaglandin generation and the roles of individual mediators and their receptors in modulating the inflammatory response. Prostaglandin biology has potential clinical relevance for atherosclerosis, the response to vascular injury and aortic aneurysm. Inflammation is the immune system’s response to infection and injury and has been implicated in the pathogeneses of arthritis, cancer and stroke, as well as in neurodegenerative and cardiovascular disease. Inflammation is an intrinsically beneficial event that leads to removal of offending factors and restoration of tissue structure and physiological function. The acute phase of inflammation is characterized by the rapid influx of blood granulocytes, typically neutrophils, followed swiftly by monocytes that mature into inflammatory macrophages that subsequently proliferate and thereby affect the functions of resident tissue macrophages. This process causes the cardinal signs of acute inflammation: rubor (redness), calor (heat), tumor (swelling) and dolor (pain). Once the initiating noxious stimulus is removed via phagocytosis, the inflammatory reaction can decrease and resolve. During the resolution of inflammation, granulocytes are eliminated and macrophages and lymphocytes return to normal pre-inflammatory numbers and phenotypes. The usual outcome of the acute inflammatory program is successful resolution and repair of tissue damage, rather than persistence and dysfunction of the inflammatory response, which can lead to scarring and loss of organ function. It may be anticipated, therefore, that failure of acute inflammation to resolve may predispose to auto-immunity, chronic dysplastic inflammation and excessive tissue damage (1). Prostaglandins play a key role in the generation of the inflammatory response. mango seriously this is the undisclosed. what was the document? www.ncbi.nlm.nih.gov/pmc/articles/PMC3081099/They already have one of these, Treprostinil, what would the other one be? What are you thinking it may be and indicated for? help me out here. it did occur to me that treprosrinil is a prostaglandin however, I did not find that. Abstract: A prostaglandin composition and method for treating pulmonary arterial hypertension is disclose. The composition is based on diketopiperazine for pulmonary inhalation. I finally found it. www.drugbank.ca/categories/DBCAT000353 |
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Post by mango on Dec 19, 2019 16:32:26 GMT -5
They already have one of these, Treprostinil, what would the other one be? What are you thinking it may be and indicated for? help me out here. it did occur to me that treprosrinil is a prostaglandin however, I did not find that. Abstract: A prostaglandin composition and method for treating pulmonary arterial hypertension is disclose. The composition is based on diketopiperazine for pulmonary inhalation. I finally found it. www.drugbank.ca/categories/DBCAT000353It is in the patent claims yo We claim: 1. A pharmaceutical dry powder composition comprising a treprostinil dose in an amount of up to 200 pg and one or more pharmaceutically acceptable salt thereof and a pharmaceutically acceptable carrier and/or excipients. |
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Post by peppy on Dec 19, 2019 17:45:11 GMT -5
help me out here. it did occur to me that treprosrinil is a prostaglandin however, I did not find that. Abstract: A prostaglandin composition and method for treating pulmonary arterial hypertension is disclose. The composition is based on diketopiperazine for pulmonary inhalation. I finally found it. www.drugbank.ca/categories/DBCAT000353It is in the patent claims yo We claim: 1. A pharmaceutical dry powder composition comprising a treprostinil dose in an amount of up to 200 pg and one or more pharmaceutically acceptable salt thereof and a pharmaceutically acceptable carrier and/or excipients. I saw that. [0016] Parenteral prostacyclin analogs have been the most widely studied. Intravenous epoprostenol was the first US Food and Drug Administration (FDA)-approved treatment for PAH (approved in 1995). However, due to its extremely short half-life (3-5 min), epoprostenol needs to be delivered as a continuous intravenous infusion through an indwelling catheter, with the risk of rebound PAH and acute right heart failure in case of infusion interruption. Furthermore, due to the inherent chemical instability of epoprostenol at room temperature and neutral pH (room temperature stability <8 hours), ice packs are needed to slow decomposition throughout the infusion period. A thermostable epoprostenol preparation for infusion (Veletri®), which does not require cooling, has been approved for use by the FDA. However, serious adverse events related to the delivery' system include pump malfunction, local site infection, catheter obstruction, and sepsis continues to be a barrier for its use. [0017] Treprostinil, is a longer-acting tricyclic benzidine analogue of epoprostenol with a terminal elimination half-life of approximately 2 to 4 hours and a distribution half-life of approximately 40 minutes. Unlike epoprostenol, Treprostinil is chemically stable at room temperature allowing it to be administered at ambient temperature and overcomes some of the limitations associated with epoprostenol therapy. Treprostinil causes vasodilation of pulmonary and systemic arterial vascular beds, and inhibits platelet aggregation by binding to prostacyclin IP receptors located on the surface of vascular smooth muscle cells and platelets. Treprostinil (Remodulin®) was first approved by the FDA in 2002 for adults with WHO group 1 PAH and functional class II to class IV status for continuous subcutaneous infusion and is marketed by United Therapeutics (Silver Spring, MD). In a pivotal 12 week randomized, controlled trial of 470 patients, subcutaneous Treprostinil significantly improved exercise capacity compared with placebo. The most common adverse events noted in subcutaneous infusion of Treprostinil-treated patients were infusion site pain. Read more: mnkd.proboards.com/thread/8056/mnkd-patents?page=20#ixzz68azlkjxR |
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Post by falconquest on Dec 19, 2019 17:51:29 GMT -5
help me out here. it did occur to me that treprosrinil is a prostaglandin however, I did not find that. Abstract: A prostaglandin composition and method for treating pulmonary arterial hypertension is disclose. The composition is based on diketopiperazine for pulmonary inhalation. I finally found it. www.drugbank.ca/categories/DBCAT000353It is in the patent claims yoWe claim: 1. A pharmaceutical dry powder composition comprising a treprostinil dose in an amount of up to 200 pg and one or more pharmaceutically acceptable salt thereof and a pharmaceutically acceptable carrier and/or excipients. yo? I must be getting old!  |
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Post by mango on Jan 6, 2020 15:54:06 GMT -5
Fresh Patent Published 1/1/2020 MICROCRYSTALLINE DIKETOPIPERAZINE COMPOSITIONS, METHODS FOR PREPARATION AND USE THEREOFApplication Date:14.03.2014 Publication Date:01.01.2020 Applicants:MANNKIND CORP Inventors:WILSON BRYAN R GUARNERI JOSEPH J GRANT MARSHALL L patentscope.wipo.int/search/en/detail.jsf?docId=EP279872404&_cid=P20-K52X2V-26288-1——————————— Claims 7. The dry powder composition of claim 4, wherein the one or more active ingredients is at least one of insulin or an analog thereof, a parathyroid hormone or an analog thereof, calcitonin, glucagon, glucagon-like peptide 1, oxyntomodulin, peptide YY, leptin, a cytokine, a lipokine, an enkephalin, a cyclosporin, an anti-IL-8 antibody, an IL-8 antagonist including ABX-IL-8; a prostaglandin including PG-12, an LTB receptor blocker including LY2931 1, BIIL 284 and CP105696; a triptan such as sumatriptan or palmitoleate, a growth hormone or analogs thereof, a parathyroid hormone related peptide (PTHrP), ghrelin, obestatin, enterostatin, granulocyte macrophage colony stimulating factor (GM-CSF), amylin, amylin analogs, clopidogrel, PPACK (D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone), adiponectin, cholecystokinin (CCK), secretin, gastrin, motilin, somatostatin, brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), IGF-1, growth hormone releasing factor (GHRF), integrin beta-4 precursor (ITB4) receptor antagonist, analgesics, nociceptin, nocistatin, orphanin FQ2, CGRP, angiotensin, substance P, neurokinin A, a pancreatic polypeptide, a neuropeptide Y, a delta-sleep-inducing peptide, or a vasoactive intestinal peptide. |
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