15 results about "Adrenergic agonist" patented technology

The present disclosure relates to compositions, formulations, and associated methods for treating neurodegenerative diseases, wherein the compositions include an alpha-1 adrenergic agonist, such as midodrine, and an alpha-2A adrenergic agonist, such as dexmedetomidine. Upon administering to a human subject, the alpha-2A adrenergic agonist crosses the subject's blood-brain barrier thereby acting upon the subject's central nervous system, whereas the alpha-1 adrenergic agonist does not cross the subject's blood-brain barrier. The alpha-1 adrenergic agonist minimizes or eliminates the systemic vascular effects induced by the alpha-2A adrenergic agonist that causes the negative cerebral autoregulatory response, thereby enabling the alpha-2A adrenergic agonist to increase glymphatic flow in the subject's brain.

Provided are methods for treating trigeminal nerve pain in a subject in need thereof. The method may include administering to the subject by perineural injection of the trigeminal nerve a therapeutically effective amount of a composition comprising an alpha-2 adrenergic agonist, such as guanfacine. The composition may further comprise lidocaine.

To provide a composition or the like for treating agitation or signs of agitation.SOLUTION: The present invention discloses a method of treating agitation or signs of agitation in a subject comprising sublingual administration of an effective amount of an alpha-2 adrenergic agent, more particularly dexmedetomidine or a pharmaceutically acceptable salt thereof. The method is particularly suitable for the treatment of agitation associated with neurodegenerative diseases and / or neuropsychiatric diseases. The present invention also discloses sublingual administration of an alpha-2 adrenergic agent, more specifically dexmedetomidine or a pharmaceutically acceptable salt thereof, at a dose that is effective to treat agitation or the symptoms of agitation but does not cause significant sedation in the subject.SELECTED DRAWING: Figure 1A

Provided are methods for treating trigeminal nerve pain in a subject in need thereof. The method may include administering to the subject by perineural injection of the trigeminal nerve a therapeutically effective amount of a composition comprising an alpha-2 adrenergic agonist, such as guanfacine. The composition may further comprise lidocaine.

The present invention provides a method for reducing the level of an alpha2 adrenergic receptor agonist in a patient. The present invention also provides a method for preventing or treating an excess of an alpha2 adrenergic receptor agonist alone or in combination with other abuse drugs in a patient.

The compounds and methods of the present disclosure exhibit induce Ucp1 transcription, enhance of mitochondrial respiration, activate protein kinase A, increase lipolysis, and increase p38 MAPK phosphorylation in cells, particularly brown adipocytes and white adipocytes. They also protect primary cardiomyocytes against hypertrophy induced by adrenergic agonists. Such compounds and methods are useful in the treatment and prevention of conditions such as obesity and associated complex metabolic, endocrine, and hemodynamic changes, as well as related conditions as dyslipidemias, cardiovascular disease, and type 2 diabetes.

The present disclosure relates to compositions, formulations, and associated methods for treating neurodegenerative diseases, wherein the compositions include an alpha-1 adrenergic agonist, such as midodrine, and an alpha-2A adrenergic agonist, such as dexmedetomidine. Upon administering to a human subject, the alpha-2A adrenergic agonist crosses the subject's blood-brain barrier thereby acting upon the subject's central nervous system, whereas the alpha-1 adrenergic agonist does not cross the subject's blood-brain barrier. The alpha-1 adrenergic agonist minimizes or eliminates the systemic vascular effects induced by the alpha-2A adrenergic agonist that causes the negative cerebral autoregulatory response, thereby enabling the alpha-2A adrenergic agonist to increase glymphatic flow in the subject's brain.

The present invention relates to salts of budesonide 21-phosphate with β2 adrenergic agonists, preferably with formoterol, pharmaceutical compositions containing the same and the use thereof in the treatment of respiratory inflammatory pathologies, obstructive pathologies and allergen-induced airway dysfunctions. The invention further relates to the process for preparing said salts.

To provide a non-surgical alternative to blepharoplasty for treatment and cosmetic applications.SOLUTION: To provide cosmetic and therapeutic compositions of alpha-adrenergic agents. The compositions of the disclosure may be used for topical, transdermal or parenteral administration to the eye or eyelid. The compositions of the present disclosure may be used cosmetically to improve the appearance of the eye or therapeutically to treat ptosis.SELECTED DRAWING: None

Provided herein are methods of stabilizing blood pressure in severe sepsis / septic shock and other types of distributive shock using TRPV1 agonists. Also provided are pharmaceutical formulations for increasing blood pressure in septic shock the formulation including at least one TRPV1 agonist in a dosage form for parenteral administration, wherein the TRPV1 agonist is selected from capsaicin, daphnane TRPV1 agonists, vanillotoxin, N-oleoyl dopamine, N-arachidonyl dopamine, BrP-LPA, and derivatives and analogues thereof. Also provided are TRPV1 agonists co-lyophilized with adrenergic agonists and / or angiotensins in a dosage form for reconstitution and parenteral administration.

The present disclosure is directed to chemical compounds and to the use of such compounds in the treatment of diseases associated with an adrenergic receptor.

The present disclosure relates to compositions, formulations, and associated methods for treating neurodegenerative diseases, wherein the compositions include an alpha-1 adrenergic agonist, such as midodrine, and an alpha-2A adrenergic agonist, such as dexmedetomidine. Upon administering to a human subject, the alpha-2A adrenergic agonist crosses the subject's blood-brain barrier thereby acting upon the subject's central nervous system, whereas the alpha-1 adrenergic agonist does not cross the subject's blood-brain barrier. The alpha-1 adrenergic agonist minimizes or eliminates the systemic vascular effects induced by the alpha-2A adrenergic agonist that causes the negative cerebral autoregulatory response, thereby enabling the alpha-2A adrenergic agonist to increase glymphatic flow in the subject's brain.

A co-drug or a pharmaceutical salt thereof includes a muscarinic agonist moiety and an alpha2 adrenergic agonist moiety. The muscarinic agonist moiety and the alpha2 adrenergic agonist moiety are connected covalently via a linker, and the link includes an ester bond, an amide bond, a carbamate bond, or a combination thereof.

The present disclosure provides methods of treating an individual for a muco-obstructive, the methods including: administering to the individual a b-adrenergic agonist or an adenylate cyclase activator, in combination with a cholinergic agonist to treat the individual for the muco-obstructive disorder.

The present disclosure relates generally to various forms and compositions useful as beta adrenergic agonists and the use of the various forms and compositions in the treatment of diseases associated with adrenergic receptors. In one aspect, the present disclosure provides: crystalline solid forms of Compound 1 selected from Form A and Form B; and salt forms of Compound 1.