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Formulations and methods for treating amyloidosis

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Formulations and methods for treating amyloidosis


Methods, formulations, and compositions for the treatment of amyloidosis are described.
Related Terms: Amyloidosis

Browse recent Kiacta Sarl patents - ,
Inventors: Denis Garceau, Wendy Hauck, Richard Briand
USPTO Applicaton #: #20120270939 - Class: 514517 (USPTO) - 10/25/12 - Class 514 
Drug, Bio-affecting And Body Treating Compositions > Designated Organic Active Ingredient Containing (doai) >(o=)n(=o)-o-c Containing (e.g., Nitrate Ester, Etc.) >Carbon Bonded To -ncx Or -xcn (e.g., Cyanate, Thiocyanate Or Isothiocyanate, Etc.) (x Is Chalcogen) >S-x-c Containing (e.g., Sulfates, Etc.) (x Is Chalcogen)

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The Patent Description & Claims data below is from USPTO Patent Application 20120270939, Formulations and methods for treating amyloidosis.

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RELATED APPLICATIONS

This application is a continuation of U.S. application Ser. No. 11/405,348 filed Apr. 17, 2006, which claims the benefit Under 35 U.S.C. §119(e) of U.S. Provisional Application No. 60/671,866, filed Apr. 15, 2005, which are incorporated herein by reference in their entireties and for all purposes.

BACKGROUND OF THE INVENTION

Amyloidosis is the generic term for a number of diseases related by extracellular deposition of insoluble fibrillar proteins (amyloid) in specific organs, which eventually leads to the failure of the involved organs. R. H. Falk et al, The Systemic Amyloidosis, 337 N ENGL J MED 898-909 (1997), P. N. Hawkins, Amyloidosis, 9 BLOOD REV 135-42 (1995), J. D. Sipe, Amyloidosis, 31 CR REV CE1N LAB SC 1325-54 (1994); A. S. Cohen, Amyloidosis, 40(2) BULL RHEUM DISEASES 1-12 (1991). Amyloid deposits can remain limited to one organ (localized amyloidosis) or may be more broadly distributed (systemic amyloidosis). Systemic amyloidoses are generally classified into four types based on the nature of the fibrillar deposits: (i.) idiopathic or primary amyloidosis (AL amyloidosis); (ii.) reactive, secondary or amyloid A (AA) amyloidosis; (iii.) familial amyloidotic polyneuropathy; and (iv.) dialysis-associated amyloidosis. Though diverse in their occurrence, all amyloid deposits have common morphologic properties, stain with specific dyes (e.g., Congo red), and have a characteristic birefringent appearance in polarized light after staining. They also share common ultrastructural features and common X-ray diffraction and infrared spectra.

AA amyloidosis is thought to be related to amyloid A (AA) protein formed from the precursor serum amyloid A (SAA), an acute phase protein produced and secreted by hepatocytes in response to inflammation. AA amyloidosis is associated with chronic inflammatory conditions (e.g. rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, etc.), chronic infections (e.g., tuberculosis, osteomyelitis etc.), and hereditary fevers, e.g., Familial Mediterranean Fever (R. H. Falk et al., 337 N ENGL J MED 898-909 (1997), A. S. Cohen, 40(2) BULL RHEUM DISEASES 1-12 (1991), G. Grateau, 12 CURRENT OPINION IN RHEUMATOL 61-64 (2000)). Rheumatoid arthritis is the major cause of AA amyloidosis in Western Europe and North America (M. Skinner Amyloidosts, CURRENT THERAPY IN ALLERGY, IMMUNOLOGY, AND RHEUMATOLOGY 235-40 (Mosby-Year Book Inc., 1996), M. A. Gertz, Secondary amyloidosis, 232 J INT MED 517-18 (1992)).

AA amyloidosis mainly affects parenchymatous organs, such as, kidneys, spleen, liver, and adrenals. The most common clinical feature of AA amyloidosis is renal dysfunction manifested as nephrotic-range proteinuria or renal insufficiency at the time of diagnosis. End-stage renal failure is the cause of death in 40-60% of cases (M. Skinner Amyloidosis, CURRENT THERAPY IN ALLERGY, IMMUNOLOGY, AND RHEUMATOLOGY 235-40 (Mosby-Year Book Inc., 1996), M. A. Gertz, 232 J INT MED 517-18 (1992), M. A. Gertz and R. A. Kyle, 70 MEDICINE 246-256 (1991)). Gastrointestinal involvement is also frequent and is usually manifested as chronic diarrhea, body weight loss and malabsorption. Enlargement of the liver and spleen may also occur in some subjects. Cardiac involvement is rare and occurs late in the disease. The median survival time from diagnosis varies from 2 to 8 years depending on the stage of the disease at time of diagnosis (M. A. Gertz and R. A. Kyle, 70 MEDICINE 246-256 (1991)).

AA amyloidosis is usually seen associated with chronic infection (such as tuberculosis) or chronic inflammation (such as rheumatoid arthritis or hereditary fevers). A familial form of AA amyloidosis is seen Familial Mediterranean Fever (FMF). This familial type of amyloidosis is genetically inherited and is found in specific population groups. In both AL and AA amyloidosis, deposits are found in several organs and are thus considered systemic amyloid diseases.

“Localized amyloidoses” are those that tend to involve a single organ system. Different amyloids are also characterized by the type of protein present in the deposit. For example, neurodegenerative diseases such as scrapie, bovine spongiform encephalitis, Creutzfeldt-Jakob disease, and the like are characterized by the appearance and accumulation of a protease-resistant form of a prion protein (referred to as AScr or PrP-27) in the central nervous system. Similarly, Alzheimer\'s disease, another neurodegenerative disorder, is characterized by neuritic plaques and neurofibrillary tangles. In this case, the amyloid plaques found in the parenchyma and the blood vessel is formed by the deposition of fibrillar Aβ amyloid protein. Other diseases such as adult-onset diabetes (type II diabetes) are characterized by the localized accumulation of amyloid fibrils in the pancreas.

Once these amyloids have formed, there is no known, widely accepted therapy or treatment which significantly dissolves amyloid deposits in situ, prevents further amyloid deposition or prevents the initiation of amyloid deposition.

Each amyloidogenic protein has the ability to undergo a conformational change and to organize into β-sheets and form insoluble fibrils which may be deposited extracellularly or intracellularly. Each amyloidogenic protein, although different in amino acid sequence, has the same property of forming fibrils and binding to other elements such as proteoglycan, amyloid P and complement component. Moreover, each amyloidogenic protein has amino acid sequences which, although different, show similarities such as regions with the ability to bind to the glycosaminoglycan (GAG) portion of proteoglycan (referred to as the GAG binding site) as well as other regions which promote β-sheet formation. Proteoglycans are macromolecules of various sizes and structures that are distributed almost everywhere in the body. They can be found in the intracellular compartment, on the surface of cells, and as part of the extracellular matrix. The basic structure of all proteoglycans is comprised of a core protein and at least one, but frequently more, polysaccharide chains (GAGs) attached to the core protein. Many different GAGs have been discovered including chondroitin sulfate, dermatan sulfate, keratan sulfate, heparin, and hyaluronan.

Some GAG mimetics are known to be useful for inhibiting amyloid deposition and/or treating some forms of amyloidosis. See WO 94/22437, WO 96/28187, and WO 00/64420.

SUMMARY

OF THE INVENTION

In one embodiment, the invention pertains to a method of treating or preventing AA amyloidosis in a target subject, by administering to the target subject a therapeutically effective amount of a compound of the formula:

Y—(CH2)n—[CH2Y]m  (I)

wherein Y is SO3X or OSO3X independently chosen for each occurrence; X is cationic group independently chosen for each occurrence; n is 1, 2, 3 or 4; and m is 1 or 2, such that the AA amyloidosis is treated or prevented, while maintaining an acceptable tolerance index (ATI) for a parameter associated with renal impairment (PRI). Furthermore, in this embodiment, the target subject is being treated for AA amyloidosis and has or is susceptible to a parameter associated with renal impairment. In a further embodiment the compound of formula (I) is 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt.

In another embodiment, the invention includes a method of treating or preventing AA amyloidosis in a target subject, by administering to the target subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the AA amyloidosis is treated or prevented while maintaining an acceptable tolerance index (ATI) for a parameter associated with gastrointestinal impairment (PGI). Furthermore, in this embodiment, the target subject is being treated for AA amyloidosis and has or is susceptible to a parameter associated with gastrointestinal impairment.

In another further embodiment, the invention also pertains to a method of treating or preventing an amyloid related disease in a subject by administering to a subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, at a dosage selected based upon creatinine clearance rate, such that the amyloid related disease is treated or prevented.

The invention also pertains, at least in part, to a method for treating or preventing AA amyloidosis in a subject, by administering to the subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, which is administered in a dosage, such that an effective exposure is provided in a subject, for example, as measured by, e.g., AUC, Cmax, AUCss, Css, Tmax, etc.

In addition, the invention also pertains to a method of stabilizing or improving renal and/or gastrointestinal function in a subject. The method includes administering to a subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt.

In another embodiment, the invention pertains to a method of treating or preventing AA amyloidosis in a subject. The method includes administering to a subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a second agent such that AA amyloidosis is treated or prevented.

In yet another embodiment, the invention pertains, at least in part, to a method of increasing the oral bioavailability of a compound in a subject, by administering to a subject a therapeutically effective amount of the compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in a pharmaceutical composition without food such that the oral bioavailability of the compound in the subject is increased.

The invention also pertains, at least in part, to a method of treating an inflammatory disease in a subject, by administering to a subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a second agent such that said inflammatory disease is treated in the subject.

The invention also pertains, at least in part, to a method of treating a hereditary fever in a subject, by administering to a subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a second agent such that said hereditary fever is treated in the subject.

The invention also pertains, at least in part, to a method for treating rheumatoid arthritis in a subject. The method includes administering to a subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a second agent.

In addition, the invention also includes a method of treating a malignant neoplasm in a subject. The method includes administering to a subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a second agent such that the malignant neoplasm is treated in the subject.

In a further embodiment, the invention pertains, at least in part, to a method of treating a chronic infection, e.g., microbial or viral, in a subject. The method includes administering to a subject in need thereof, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a second agent such that the chronic infection is treated in the subject.

In another further embodiment, the invention pertains at least in part to method of stabilizing or improving renal function or delaying progression of renal disease in a subject having an inflammatory disorder, a malignant neoplasm, a chronic infection or a hereditary fever. The method includes administering to the subject a therapeutically effective amount of 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, such that renal function is stabilized or improved or progression of renal disease is delayed.

In another embodiment, the invention pertains, at least in part, to a method for preventing or delaying progression to ESRD/dialysis in a subject having AA amyloidosis. The method includes administering to the subject, e.g., a subject having AA amyloidosis, a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that progression to ESRD/dialysis is delayed or prevented.

In another embodiment, the invention pertains, at least in part, to a method for preventing or delaying the time to the doubling of serum creatinine in a subject having AA amyloidosis. The method includes administering to the subject a therapeutically effective amount of a compound, of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the time to the doubling of serum creatinine is delayed or prevented.

In yet another embodiment, the invention pertains, at least in part, to a method for preventing or delaying the time to at least a 50% decrease in creatinine clearance in a subject having AA amyloidosis. The method includes administering to a subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the time to the at least a 50% decrease in creatinine clearance is delayed or prevented.

In another embodiment, the invention pertains, at least in part, to a method for decreasing the time to at least a 50% increase in creatinine clearance in a subject having AA amyloidosis. The method includes administering to the subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the time to the at least 50% increase in creatinine clearance is decreased.

In yet another embodiment, the invention includes a method for reducing the rate of progression of renal disease as measured by the slope of creatinine clearance in a subject having AA amyloidosis. The method includes administering to the subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the rate of progression of renal disease is reduced.

In another embodiment, the invention pertains, at least in part, to a method for stabilizing or reducing proteinuria in a subject having AA amyloidosis. The method includes administering to the subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the proteinuria in said subject is stabilized or reduced.

In yet another embodiment, the invention includes a method for stabilizing renal function or delaying progression of renal disease in a subject having AA amyloidosis. The method includes administering to the subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that renal function is stabilized or progression of renal disease is delayed. In one aspect, progression of renal disease may be measured by a 50% decrease in creatinine clearance (CrCI), doubling of serum creatinine (SCr), and/or progression to ESRD.

In yet another further embodiment, the invention pertains, at least in part, to a method for treating renal impairment in a subject having AA amyloidosis. The method includes administering to the subject a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, such that the renal impairment is treated.

The invention also pertains, at least in part, to a pharmaceutical composition comprising a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, and a second agent.

In a further embodiment, the invention pertains to a packaged pharmaceutical composition. The packaged pharmaceutical composition includes a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, packaged in combination with a label or insert advising that the composition be administered in combination with a second agent.

In yet another further embodiment, the invention pertains to a packaged pharmaceutical composition, which includes a therapeutically effective amount of a second agent packaged in combination with a label or insert advising that the composition be administered in combination with a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt.

In yet another embodiment, the invention pertains to a packaged pharmaceutical composition, which includes a container holding a pharmaceutical composition comprising a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in combination with a label or insert advising that the composition be administered without food.

In yet another embodiment, the invention pertains to a pharmaceutical formulation for treating AA amyloidosis. The formulation comprising a therapeutically effective amount of a compound of formula (I), e.g., 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof, e.g. a disodium salt, in a formulation, wherein the formulation has at least one favorable biological property (FBP) upon administration to the subject.

The invention also pertains, at least in part, to an anti-amyloidogenic agent in a formulation, wherein the anti-amyloidogenic agent-containing formulation is equivalent to a standard formulation predetermined to have at least one favorable biological property upon administration to a subject such that it is a biologically favorable formulation.

In another embodiment, the invention also includes a pharmaceutical formulation, which comprising a compound of formula (I), and one or more pharmaceutically acceptable carriers. In this embodiment, the pharmaceutical formulation, when administered once to a subject in need thereof, provides a Cmax of about 200 to about 2000 ng/mL.

In yet another embodiment, the invention also pertains to a pharmaceutical formulation, comprising a compound of formula (I), and one or more pharmaceutically acceptable carriers. In this embodiment, the pharmaceutical formulation, when administered to a subject in need thereof, provides an AUC∞ about 2,000 to about 44,000 ng/mL.

The invention also pertains, at least in part, to a method of administering a compound to a subject in need thereof. The method includes administering a compound of formula (I) to the subject in an amount sufficient to achieve a Cmax of about 200 to about 3,400 ng/mL. The Cmax may occur about 0.25 to about 9.00 hours after administration.

In another embodiment, the invention also pertains, at least in part, to a method of administering a compound of formula (I) to a subject in need thereof. The method includes administering a compound of formula (I) to the subject in an amount sufficient to achieve an AUC∞ of about 2,000 to about 44,000 ng/mL.

In yet another embodiment, the invention pertains to a pharmaceutical formulation, which comprises a 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof and one or more pharmaceutically acceptable carriers. The pharmaceutical formulation provides a Cmax of about 200 to about 2000 ng/mL, when administered once to a subject in need thereof.

In yet another embodiment, the invention also includes a pharmaceutical formulation, which comprises 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof and one or more pharmaceutically acceptable carriers. The pharmaceutical formulation provides a AUC∞ of about 2,000 to about 44,000 ng/mL, when administered to a subject in need thereof.

In yet another embodiment, the invention also pertains to a method of administering 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof to a subject in need thereof. The method includes administering 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof to a subject in an amount sufficient to achieve a Cmax of about 200 to about 3,400 ng/mL about 0.25 to about 9.00 hours after administration.

In another embodiment, the invention also pertains to a method of administering 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof to a subject in need thereof, by administering 1,3-propanedisulfonic acid or a pharmaceutically acceptable salt thereof to the subject in an amount sufficient to achieve an AUC∞ of about 2,000 to about 44,000 ng/mL.

In yet another embodiment, the invention pertains, at least in part, to a pharmaceutical formulation. The pharmaceutical formulation comprises an active agent (e.g., 1,3-propanedisulfonic acid, disodium salt (also referred to as PDS) in an amount effective to treat or prevent AA amyloidosis, and a pharmaceutically acceptable carrier, wherein, when the formulation is orally administered to a healthy subject, a mean plasma concentration profile of the active agent having a mean AUC∞ of about from 2900 to about 9000 ng·h/mL±20% and a mean Cmax of about from 450 to about 2150 ng/mL±20% is achieved.

In yet another further embodiment, the invention also pertains, at least in part, to a pharmaceutical formulation, which comprises an active agent (e.g., PDS) in an amount effective to treat or prevent AA amyloidosis, and a pharmaceutically acceptable carrier, wherein, when the formulation is orally administered to a healthy subject, a mean plasma concentration profile of the active agent having a mean AUC∞ of from about 2,900 to about 9,000 ng·h/mL±20% is achieved.

In yet another further embodiment, the invention pertains to a pharmaceutical formulation, which comprises an active agent (e.g., PDS) in an amount effective to treat or prevent AA amyloidosis, and a pharmaceutically acceptable carrier, wherein, when the formulation is orally administered to a healthy subject, a mean plasma concentration profile of the active agent having a mean Cmax of about from 450 to about 2150 ng/mL±20% is achieved.

In yet another further embodiment, the invention pertains, at least in part, to a pharmaceutical formulation, comprising an active agent (e.g., PDS), and a pharmaceutically acceptable carrier, wherein, when the formulation is orally administered to a subject having AA amyloidosis: in a dose of 400 mg of the active agent to a subject having a creatinine clearance rate of less than about 30 ml/min, a mean plasma concentration profile of the active agent having a mean AUC∞ of about 10,000-12,000 ng·h/mL±20%, and a mean Cmax of about 800-900 ng/mL±20% is achieved; or in a dose of 800 mg of the active agent to a subject having a creatinine clearance rate of about 30 to about 80 mL/min, a mean plasma concentration profile of the active agent having a mean AUC∞ of about 9,000-10,500 ng·h/mL±20%, and a mean Cma, of about 750-875 ng/mL±20% is achieved; or in a dose of 1200 mg of the active agent to a subject having a creatinine clearance rate of greater than about 80 mL/min, a mean plasma concentration profile of the active agent having a mean AUC∞ of about 5,000-6,000 ng·h/mL±20%, and a mean Cmax of about 800-925 ng/mL±20% is achieved.



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stats Patent Info
Application #
US 20120270939 A1
Publish Date
10/25/2012
Document #
File Date
10/23/2014
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Amyloidosis


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