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In fact an individual suffering from an ischemic insult continues suffering injuries well after circulation is restored. In rats it has been shown that neurons often die a full 24 hours after blood flow returns. Some theorize that this delayed reaction derives from the various inflammatory immune responses that occur during reperfusion. Beyond this, reperfusion also increases free radical production. Many now suspect it is because hypothermia reduces both intracranial pressure and free radical production that hypothermia improves patient outcome following a blockage of blood flow to the brain.
There are some preliminary studies that seem to indicate that treatment with hydrogen sulfide H 2 S can have a protective effect against reperfusion injury.
In addition to its well-known immunosuppressive capabilities, the one-time administration of cyclosporin at the time of percutaneous coronary intervention PCI has been found to deliver a 40 percent reduction in infarct size in a small group proof of concept study of human patients with reperfusion injury published in The New England Journal of Medicine in Cyclosporin has been confirmed in studies to inhibit the actions of cyclophilin D, a protein which is induced by excessive intracellular calcium flow to interact with other pore components and help open the MPT pore.
Inhibiting cyclophilin D has been shown to prevent the opening of the MPT pore and protect the mitochondria and cellular energy production from excessive calcium inflows.
Both studies found there is no statistical difference in outcome with cyclosporin administration. Reperfusion leads to biochemical imbalances within the cell that lead to cell death and increased infarct size. More specifically, calcium overload and excessive production of reactive oxygen species in the first few minutes after reperfusion set off a cascade of biochemical changes that result in the opening of the so-called mitochondrial permeability transition pore MPT pore in the mitochondrial membrane of cardiac cells.
The opening of the MPT pore leads to the inrush of water into the mitochondria, resulting in mitochondrial dysfunction and collapse.
Upon collapse, the calcium is then released to overwhelm the next mitochondria in a cascading series of events that cause mitochondrial energy production supporting the cell to be reduced or stopped completely.
The cessation of energy production results in cellular death. Protecting mitochondria is a viable cardioprotective strategy. In , an editorial in the New England Journal of Medicine called for more studies to determine if cyclosporin can become a treatment to ameliorate reperfusion injury by protecting mitochondria. Results of that study were announced in and indicated that "intravenous ciclosporin did not result in better clinical outcomes than those with placebo and did not prevent adverse left ventricular remodeling at 1 year".
TRO is a new cardioprotective compound that was shown to inhibit the MPT pore and reduce infarct size after ischemia-reperfusion. It was developed by Trophos company and currently is in Phase I clinical trial. Recent investigations suggest a possible beneficial effect of mesenchymal stem cells on heart and kidney reperfusion injury.
Superoxide dismutase is an effective anti-oxidant enzyme which converts superoxide anions to water and hydrogen peroxide. Recent researches have shown significant therapeutic effects on pre-clinical models of reperfusion injury after ischemic stroke. A series of studies published in the Journal of Cardiovascular Pharmacology suggest that Metformin may prevent cardiac reperfusion injury by inhibition of Mitochondrial Complex I and the opening of MPT pore and in rats.
From Wikipedia, the free encyclopedia. The Journal of Pathology. American Journal of Surgery. The above patents, publications, and references are incorporated by reference in their entirety. In some instances, framework region FR residues of the human immunoglobulin are replaced by corresponding non-human residues. Furthermore, humanized antibodies may comprise residues that are not found in the recipient antibody or in the donor antibody.
These modifications may be made to further refine antibody performance. In general, a humanized antibody will comprise substantially all of at least one, and typically two, variable domains, in which all or substantially all of the hypervariable loops correspond to those of a non-human immunoglobulin, and all or substantially all of the FRs are those of a human immunoglobulin sequence. The humanized antibody optionally will also comprise at least a portion of an immunoglobulin constant region Fc , typically that of a human immunoglobulin.
For further details, see Jones et al. See also the following review articles and references cited therein: Vaswani and Hamilton, Ann.
Such techniques include screening human-derived combinatorial libraries, such as phage display libraries see, e. This definition of a human antibody specifically excludes a humanized antibody comprising antigen-binding residues from a non-human animal.
All known types of such antibodies are within the scope of the invention. Exemplary antibodies include those that bind to growth factors, cytokines, lymphokines, cell surface receptors, enzymes, vascular endothelial growth factors, fibroblast growth factors, and antibodies to their respective receptors.
Other exemplary antibodies include monoclonal antibodies directed to receptor-IgG Fc fusion proteins, and glycoproteins. Therapeutic compounds to be used in the invention are known in the art and are disclosed by way of example in U. Additionally, the invention contemplates conjugates of inhibitors or antagonists of naturally-occurring or non-naturally occurring antibodies in a subject that cause autoimmune diseases or undesirable inflammatory conditions. Some aspects of the assembly of carriers utilizes chemical methods that are well-known in the art.
Methods of producing PEG molecules with some vitamins and other therapeutic compounds linked to them follows these and other chemical methods known in the art. Several coupling methods are contemplated and include, for example, NHS coupling to amine groups such as a lysine residue on a peptide, maleimide coupling to sulfhydryl group such as on a cysteine residue, iodoacetyl coupling to a sulfhydryl group, pyridyldithiol coupling to a sulfhydryl group, hydrazide for coupling to a carbohydrate group, aldehyde for coupling to the N-terminus, or tetrafluorophenyl ester coupling that is known to react with primary or secondary amines.
Other possible chemical coupling methods are known to those skilled in the art and can be substituted.
In one embodiment, carrier compounds may be covalently or noncovalently attached to the drug. In another embodiment, the carrier compounds are separate from the drugs but are mixed together at discrete concentrations so as to become formulated into functional units.
Exemplary drug formulations of the invention include aqueous solutions, organic solutions, powder formulations, solid formulations and a mixed phase formulations.
Pharmaceutical compositions of this invention comprise any of the compounds of the present invention, and pharmaceutically acceptable salts thereof, with any pharmaceutically acceptable carrier, adjuvant or vehicle. Pharmaceutically acceptable carriers, adjuvants and vehicles that may be used in the pharmaceutical compositions of this invention include, but are not limited to, ion exchangers, alumina, aluminum stearate, lecithin, serum proteins, such as human serum albumin, buffer substances such as phosphates, glycine, sorbic acid, potassium sorbate, partial glyceride mixtures of saturated vegetable fatty acids, water, salts or electrolytes, such as protamine sulfate, disodium hydrogen phosphate, potassium hydrogen phosphate, sodium chloride, zinc salts, colloidal silica, magnesium trisilicate, polyvinyl pyrrolidone, cellulose-based substances, polyethylene glycol, sodium carboxymethylcellulose, polyacrylates, waxes, polyethylene-polyoxypropylene-block polymers, polyethylene glycol and wool fat.
Pharmaceutically acceptable salts retain the desired biological activity of the therapeutic composition without toxic side effects. The pharmaceutical compositions of this invention may be administered by transdermal, oral, parenteral, inhalation, ocular, topical, rectal, nasal, buccal including sublingual , vaginal, or implanted reservoir modes. The pharmaceutical compositions of this invention may contain any conventional, non-toxic, pharmaceutically-acceptable carriers, adjuvants or vehicles.
The term parenteral as used herein includes subcutaneous, intracutaneous, intravenous, intramuscular, intraarticular, intrasynovial, intrasternal, intrathecal, intralesional, and intracranial injection or infusion techniques. Also contemplated, in some embodiments, are pharmaceutical compositions comprising as an active ingredient, therapeutic compounds described herein, or pharmaceutically acceptable salt thereof, in a mixture with a pharmaceutically acceptable, non-toxic component.
As mentioned above, such compositions may be prepared for parenteral administration, particularly in the form of liquid solutions or suspensions; for oral or buccal administration, particularly in the form of tablets or capsules; for intranasal administration, particularly in the form of powders, nasal drops, evaporating solutions or aerosols; for inhalation, particularly in the form of liquid solutions or dry powders with excipients, defined broadly; for transdermal administration, particularly in the form of a skin patch or microneedle patch; and for rectal or vaginal administration, particularly in the form of a suppository.
The compositions may conveniently be administered in unit dosage form and may be prepared by any of the methods well-known in the pharmaceutical art, for example, as described in Remington's Pharmaceutical Sciences, 17 th ed. For oral administration, the formulation can be enhanced by the addition of bile salts or acylcarnitines.
Formulations for nasal administration may be solid or solutions in evaporating solvents such as hydrofluorocarbons, and may contain excipients for stabilization, for example, saccharides, surfactants, submicron anhydrous alpha-lactose or dextran, or may be aqueous or oily solutions for use in the form of nasal drops or metered spray. For buccal administration, typical excipients include sugars, calcium stearate, magnesium stearate, pregelatinated starch, and the like.
Delivery of modified therapeutic compounds described herein to a subject over prolonged periods of time, for example, for periods of one week to one year, may be accomplished by a single administration of a controlled release system containing sufficient active ingredient for the desired release period. Various controlled release systems, such as monolithic or reservoir-type microcapsules, depot implants, polymeric hydrogels, osmotic pumps, vesicles, micelles, liposomes, transdermal patches, iontophoretic devices and alternative injectable dosage forms may be utilized for this purpose.
Localization at the site to which delivery of the active ingredient is desired is an additional feature of some controlled release devices, which may prove beneficial in the treatment of certain disorders. In certain embodiments for transdermal administration, delivery across the barrier of the skin would be enhanced using electrodes e.
The drug can be included in single-layer drug-in-adhesive, multi-layer drug-in-adhesive, reservoir, matrix, or vapor style patches, or could utilize patchless technology. Delivery across the barrier of the skin could also be enhanced using encapsulation, a skin lipid fluidizer, or a hollow or solid microstructured transdermal system MTS, such as that manufactured by 3M , jet injectors.
Additives to the formulation to aid in the passage of therapeutic compounds through the skin include prodrugs, chemicals, surfactants, cell penetrating peptides, permeation enhancers, encapsulation technologies, enzymes, enzyme inhibitors, gels, nanoparticles and peptide or protein chaperones. The compounds, or their salts, may also be formulated in cholesterol or other lipid matrix pellets, or silastomer matrix implants.
Additional slow release, depot implant or injectable formulations will be apparent to the skilled artisan. The foregoing are incorporated by reference in their entirety. Mixing of the therapeutic compounds described herein with such a polymeric formulation is suitable to achieve very long duration of action formulations. When formulated for nasal administration, the absorption across the nasal mucous membrane may be further enhanced by surfactants, such as, for example, glycocholic acid, cholic acid, taurocholic acid, ethocholic acid, deoxycholic acid, chenodeoxycholic acid, dehdryocholic acid, glycodeoxycholic acid, cycledextrins and the like in an amount in the range of between about 0.
An additional class of absorption enhancers reported to exhibit greater efficacy with decreased irritation is the class of alkyl maltosides, such as tetradecylmaltoside Arnold, J J et al.
The pharmaceutical compositions may be in the form of a sterile injectable preparation, for example, as a sterile injectable aqueous or oleaginous suspension. This suspension may be formulated according to techniques known in the art using suitable dispersing or wetting agents such as, for example, Tween 80 and suspending agents. The sterile injectable preparation may also be a sterile injectable solution or suspension in a non-toxic parenterally-acceptable diluent or solvent, for example, as a solution in 1,3-butanediol.
Among the acceptable vehicles and solvents that may be employed are mannitol, water, Ringer's solution and isotonic sodium chloride solution. In addition, sterile, fixed oils are conventionally employed as a solvent or suspending medium. For this purpose, any bland fixed oil may be employed including synthetic mono- or diglycerides. Fatty acids, such as oleic acid and its glyceride derivatives are useful in the preparation of injectables, as are natural pharmaceutically-acceptable oils, such as olive oil or castor oil, especially in their polyoxyethylated versions.
These oil solutions or suspensions may also contain a long-chain alcohol diluent or dispersant such as Ph. Helv or a similar alcohol.
The pharmaceutical compositions of this invention may be orally administered in any orally acceptable dosage form including, but not limited to, capsules, tablets, and aqueous suspensions and solutions.
In the case of tablets for oral use, carriers which are commonly used include lactose and corn starch. Lubricating agents, such as magnesium stearate, are also typically added. For oral administration in a capsule form, useful diluents include lactose and dried corn starch.
When aqueous suspensions are administered orally, the active ingredient is combined with emulsifying and suspending agents. The pharmaceutical compositions of this invention may also be administered in the form of suppositories for rectal administration. These compositions can be prepared by mixing a compound of this invention with a suitable non-irritating excipient which is solid at room temperature but liquid at the rectal temperature and therefore will melt in the rectum to release the active components.
Such materials include, but are not limited to, cocoa butter, beeswax and polyethylene glycols. Topical administration of the pharmaceutical compositions of this invention is especially useful when the desired treatment involves areas or organs readily accessible by topical application. For application topically to the skin, the pharmaceutical composition should be formulated with a suitable ointment containing the active components suspended or dissolved in a carrier.
Carriers for topical administration of the compounds of this invention include, but are not limited to, mineral oil, liquid petroleum, white petroleum, propylene glycol, polyoxyethylene polyoxypropylene compound, emulsifying wax and water. Alternatively, the pharmaceutical composition can be formulated with a suitable lotion or cream containing the active compound suspended or dissolved in a carrier.
Suitable carriers include, but are not limited to, mineral oil, sorbitan monostearate, polysorbate 60, cetyl esters wax, cetearyl alcohol, 2-octyldodecanol, benzyl alcohol and water. The pharmaceutical compositions of this invention may also be topically applied to the lower intestinal tract by rectal suppository formulation or in a suitable enema formulation. Topical transdermal patches are also included in this invention.
The pharmaceutical compositions of this invention may be administered by nasal aerosol or inhalation. When formulated for delivery by inhalation, a number of formulations offer advantages. Adsorption of the therapeutic compound to readily dispersed solids such as diketopiperazines for example, Technosphere particles [Pfutzner, A and Forst, T, , Expert Opin Drug Deliv 2: Dosage levels of between about 0.
Typically, the pharmaceutical compositions of this invention will be administered from about 1 to about 5 times per day or alternatively, as a continuous infusion. Such administration can be used as a chronic or acute therapy. The amount of active ingredient that may be combined with the carrier materials to produce a single dosage form will vary depending upon the host treated and the particular mode of administration.
Upon improvement of a patient's condition, a maintenance dose of a compound, composition or combination of this invention may be administered, if necessary. Subsequently, the dosage or frequency of administration, or both, may be reduced, as a function of the symptoms, to a level at which the improved condition is retained when the symptoms have been alleviated to the desired level, treatment should cease. Patients may, however, require intermittent treatment on a long-term basis upon any recurrence of disease symptoms.
As the skilled artisan will appreciate, lower or higher doses than those recited above may be required. Specific dosage and treatment regimens for any particular patient will depend upon a variety of factors, including the activity of the specific compound employed, the age, body weight, general health status, gender, diet, time of administration, rate of excretion, drug combination, the severity and course of an infection, the patient's disposition to the infection and the judgment of the treating physician.
The carrier-drug conjugate, fusion or formulation provides advantages to the drug manufacturer and the patient over the unconjugated, unfused or unformulated drug. Specifically, the carrier-drug conjugate or formulation will be a more potent and longer lasting drug requiring smaller and less frequent dosing compared to the unconjugated, unfused or unformulated drug.
This translates into lowered healthcare costs and a more convenient drug administration schedule for the patient. The carrier-drug conjugate or formulation can also influence the route of injection of a drug that is normally infused by intravenous injection to now be administered via subcutaneous injection or in a transdermal delivery system. The route of administration via subcutaneous injection or transdermal delivery is most favored because they can be self-administered by patients at home.
This can improve patient compliance. In yet another aspect of the invention, the levels of DBP can be increased as part of the carrier-drug therapy. It has been reported that estrogen can increase DBP levels Speeckaert et al. It is contemplated here that levels of DBP can be increased by administration of estrogen for more effective delivery of carrier-drug conjugates. In yet another aspect of the invention, it is contemplated that the carrier can be used to deliver drugs transdermally.
Since DBP normally transports UV activated vitamin D at locations close to the surface of the skin, the use of a transdermal delivery system with the carrier becomes feasible.
In order that the invention described herein may be more fully understood, the following examples are set forth. It should be understood that these examples are for illustrative purposes only and are not to be construed as limiting this invention in any manner.
The maleimide on the carrier in this example was used to conjugate to a free cysteine on a protein or peptide in Examples 2 and 3. It is contemplated that the size of the PEG in the scaffolds of the invention are from 0.
Thus, a 2 kDa PEG was selected as a scaffold for this example. The starting materials used in this example were purchased from commercial sources: To the resulting mixture containing compound 2 was added lithium hydroxide monohydrate 4. The reaction was flushed with nitrogen and stirred at room temperature for 18 hours. Evaluation by TLC and mass spectroscopy MS indicated complete reaction with the presence of expected compound 3. The sample was further dried under a stream of nitrogen giving R 1R,3aS,7aR,E Z S hydroxymethylenecyclohexylidene ethyl-idene -7a-methyloctahydro-1H-indenyl hexanoic acid compound 3, 5.
NMR analysis revealed the presence of about 1. The sample was further dried under a stream of nitrogen to afford the target compound as a brown gum. TLC analysis ninhydrin stain of the isolated product indicated the absence of compound 4. The NMR analysis did not show an appreciable amount of methylene chloride or other solvents. As shown below, the FGFcarrier composition provides significantly improved pharmacokinetic properties when compared to a naturally-occurring FGF21, thereby making the carrier-conjugated molecule an important therapeutic compound for the treatment of diabetes.
FGF21 was expressed in E. A modified FGF21 was designed to incorporate a free cysteine residue near the amino-terminus of FGF21 to allow site-specific coupling of the protein to the carrier and a His 6 tag added for ease of purification.
The plasmid was transformed into E. Expression of the FGF21 from the pJexpress vector in the Origami strain was accomplished as follows. Cells were harvested, lysed and the supernatant collected.
The protein was affinity purified using immobilized metal affinity chromatography IMAC resin and polished by ion exchange chromatography. The conjugated protein was separated from unreacted components by ion exchange chromatography.
Samples of plasma were collected at 30 mins, 60 mins, mins, mins, mins, 24 hrs and 48 hrs. Together, the data demonstrates the utility of the carrier molecule in increasing the bioavailability and indicates that conjugated FGF21 has significant pharmacokinetic advantages over the native FGF The Vitamin D 3 -PEG-maleimide carrier as described in Example 1 was selected to be proportional in size to a kDa peptide so that conjugation might not significantly affect the bioactivity.
The conjugated peptide was separated from unreacted components by ion exchange chromatography. Rat ghrelin rGhrelin peptide and the rGhrelin-carrier conjugates were then buffer exchanged to PBS and filter sterilized using a 0. The results show significant differences in the pharmacokinetic profiles of rGhrelin and the rGhrelin-carrier conjugate FIG. Calculation of the half-life using WinNonLin revealed a 0. The data demonstrate a second example of the usefulness of the carrier molecule in increasing half-life.
Thus, ghrelin in a conjugated form is a useful therapeutic for the treatment of ghrelin-responsive diseases such as cachexia, anorexia and frailty in the elderly. The activity of the ghrelin peptide, when conjugated to a carrier, was not adversely affected by the presence of the scaffold and targeting groups. Ghrelin binds and activates the GHS-R receptor and intracellular calcium responses were assessed as an indicator of agonist activity.
Changes in intracellular calcium levels were measured for an additional sec 21 to seconds. The data represent the average of duplicate determinations. The EC50 was determined using a data analysis wizard written by GenScript. The EC50 value of ghrelin without carrier was In comparison, the carrier-conjugated ghrelin had an EC50 value of 85 nM, which is nearly identical to the control peptide.
Thus, the agonist activity of the peptide was preserved following conjugation of the carrier to the ghrelin peptide. No interference in receptor binding and activation was observed for the carrier-conjugated peptide.
NHS-reactive groups on carriers were generated for conjugation to amine groups on proteins. A 2 kDa PEG was selected as a scaffold for this example. R -Methyl 1R,3aS,7aR,E Z S tert-butyldimethylsilyl oxy methylenecy-clohexylidene ethylidene -7a-methyloctahydro-1H-in denyl hexanoate compound 1, 8. Tetrabutylammonium fluoride solution 25 mg, 0. To the resulting mixture containing compound 2, lithium hydroxide monohydrate 4. The reaction mixture was flushed with nitrogen and stirred at room temperature for 18 hr.
Evaluation by TLC and mass spectroscopy MS indicated complete reaction with the presence of the expected compound 3. The sample was further dried under a stream of nitrogen giving R 1R,3aS,7aR,E Z S hydroxymethylenecyclohexylidene ethyl-indene -7a-methyloctahydro-1H-indenyl hexanoic acid compound 3, 6. The reaction was monitored by TLC ninhydrin stain , and upon completion of the reaction, it was concentrated on a rotavap.
NMR analysis did not show an appreciable amount of methylene chloride or ether. The reaction was incomplete at this time, therefore an additional amount of compound 3 1. The sample was purified by silica gel 2 g flash chromatography. TLC analysis ninhydrin stain of the isolated product indicated the absence of compound 6. The NMR analysis revealed the presence of 1. To this solution was added lithium hydroxide monohydrate solution 0.
Evaluation by TLC indicated complete reaction with the presence of compound 8. Stock solutions were prepared: Chloroform 10 mL was added to the reaction mixture, and it was washed with water 10 mL. The infliximab-carrier conjugate of showed increased serum concentrations and bioavailability in rats when compared to infliximab alone.
A therapeutic compound carrier conjugate of the invention typically has at least 1 and could be between carrier molecules individually attached to a therapeutic compound. By using an NHS version of the carrier, more than one carrier can be attached to a therapeutic protein and this can be experimentally controlled by altering the molar ratio of carrier to target therapeutic in the reaction.
In this example, a target distribution of carriers was set as a desired parameter. By testing two different molar ratios and examining the resulting conjugates by mass spectrometry, an actual ratio was determined.
The infliximab and infliximab NHS-carrier conjugates were separated from unconjugated carrier by use of a desalting column with a 40 kDa cutoff Zeba Spin, Thermo Scientific.
Mass spectrometry was used to calculate the intact mass of infliximab in the reactions. The results show that unmodified infliximab had a mass predominantly of kDa.
The mass of the carrier-conjugated infliximab had a mass in increasing ratios with an average attachment of the 3 kDa carrier of carriers per antibody. Serum samples were collected pre-dosing and at various times from 5 min to 48 hrs post injection.
Pharmacokinetic parameters were determined using WinNonLin. The results shown in FIG. Thus, this example shows the utility of the carrier in improving the serum concentration and bioavailability of infliximab when compared to the unconjugated antibody. The foregoing description has been presented only for purposes of illustration and description.
This description is not intended to limit the invention to the precise form disclosed. It is intended that the scope of the invention be defined by the claims appended hereto.
A SumoBrain Solutions Company. Search Expert Search Quick Search. Carriers for improved drug delivery. United States Patent The invention provides carriers that enhance the absorption, half-life or bioavailability of therapeutic compounds. The carriers comprise targeting groups that bind the Vitamin D Binding protein DBP , conjugation groups for coupling the targeting groups to the therapeutic compounds, and optionally scaffolding moieties.
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