119 results about "Forskolin" patented technology

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta -adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta -adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta -adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta -adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, or forskolin is inhibited by immunosuppressants, immunophilin ligands, or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, or forskolin is inhibited by immunosuppressants, immunophilin ligands, or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

An orally or parenterally administered composition for reducing the storage of lipids in a human, the composition comprising: an effective amount of hydroxycitric acid; an effective amount of carnitine; an effective amount of biotin; an effective amount of one or more gluconeogenic substrates selected from the group consisting of: aspartate, lactate, glycerol, and a gluconeogenic amino acid or alphaketo analogue thereof; an effective amount of eicosapentanoic acid; and an effective amount of one or more ingredients selected from the group consisting of: medium chain triglycerides (MCT) with fatty acid backbones containing 6 to 14 carbon atoms or their individual fatty acid analogues or metabolic precursors, sesame seeds or derivative products, sesamin and / or its epimer episesamin, caffeine, forskolin, 7-keto dehydroepiandrosterone (7-keto DHEA), green tea extract containing epigallocatechingallate (EGCG), capsaicum, and 5-hydroxytryptophan (5-HTP). The supplement may also be combined with a food, beverage, condiment, spice or salad dressing base to provide a food, beverage, condiment, spice or salad dressing product designed to reduce lipid storage.

The present invention provides methods and compositions for the consistent and quantitative differentiation of human preadipocytes isolated from adipose tissue into adipocytes bearing biochemical, genetic, and physiological characteristics similar to that observed in isolated primary adipocytes. The methods of the invention comprise incubating isolated human preadipocytes, plated at least about 25,000 cells / cm2, in a medium containing, glucose, a cyclic AMP inducer such as isobutylmethylxanthine or forskolin, a glucocorticoid or glucocorticoid analogue, insulin or an insulin analogue and a PPARγ agonist or a RXR agonist. The compositions of the invention include media for the differentiation of human preadipocytes, human adipocytes differentiated by the methods of the invention and transfected adipocytes.The present invention also provides methods for determining the ability of a compound to affect the differentiation of human preadipocytes to adipocytes, for determining the ability of a compound to act as a PPARγ antagonist. a glucocorticoid, a glucocoticoid analogue, or an insulin analogue, for transfecting cultured human adipocytes, and as a means to identify novel polypeptides secreted from human adipocytes into the conditioned medium. The methods and compositions have use in the drug discovery of compounds having relevance to the disease states of diabetes, obesity, and cardiovascular disease and in the studies of these diseases.

Aqueous solutions of diterpenes such as Forskolin, its congeners, analogs and derivatives, up to approximately 6% concentration, are prepared using suitably substituted cyclodextrin as a solubilizing agents. In the absence of cyclodextrin, some diterpenes such as Forskolin are soluble in water only to concentrations of about 0.001%. Such aqueous solutions find applications in topical and systemic use, as pharmaceutical, cosmeceutical, nutraceutical preparations containing diterpenes such as Forskolin and congeners.

The invention discloses an inducing culture medium for inducing fibroblast to trans-differentiate into cardiac muscle cells, a method and an application of the inducing culture medium. The inducing culture medium comprises a basic culture medium and an inducing small molecular assembly which is 6TCFOW or SCFOV, wherein 6 is E61541, T is tranylcypromine, C is CHIR99021, F is forskolin, O is Dorsomorphin, W is IWR-I, S is SB431542, and V is valproic acid. The inducing culture medium can trans-differentiate the fibroblast into the cardiac muscle cells which have normal cardiac muscle cell specific molecular tags and a normal cardiac muscle function, so that a new way is provided for solving the cell source problem of the regenerative medicine.

The present invention relates to a method of producing neurons that express the enzyme tyrosine hydroxylase (TH) by subjecting neural stem cells to FGF-1, a protein kinase A activator, a protein kinase C activator, and dopamine / L-DOPA. Surprisingly, when forskolin is used as a protein kinase A activator, it requires only low levels of FGF-1 and forskolin to efficiently produce TH positive neurons from fetal or adult neural stem cells. Also provided are compositions used to produce TH positive neurons and the resulting neural cell culture, as well as a method of treating disease or conditions which are associated with dopamine neuron loss or dysfunction.

The present invention provides compositions and methods that assist in providing weight control. Compositions comprise Caffeine, an adrenergic amine (e.g. synephrine, hordenine, octopamine, tyramine and N-methyltyramine,) forskolin, Guggulsterones, an alpha-2 receptor antagonist (e.g. Yohimbine) and a vinca alkaloid (e.g. vinpocetine.) Black pepper extract may be added as well in various alternative embodiments. Methods utilizing administration of nutrient compositions are disclosed as well.

A liquid pharmaceutical preparation comprising forskolin in an amount of about 0.025 mg / ml to about 1 mg / ml of the liquid pharmaceutical preparation for promoting lean body mass in a human subject. Further, an effective amount of the liquid pharmaceutical preparation comprising forskolin is administered subcutaneously in the human subject.

The present invention relates to a method for inducing differentiation of bone marrow-derived mesenchymal stem cells into mature neurons by culturing them in an optimal medium supplemented with necessary composition. According to the pre-induction method of the invention and a method for inducing differentiation of mesenchymal stem cells into neurons by culturing them in neuronal induction media (NIM) containing butyl hydroxyanisole, forskolin and VPA, mesenchymal stem cells can be effectively differentiated into neurons or motor neurons, which thereby can be effectively used as a therapeutic agent for cell therapy for neurodegenerative diseases.

Methods and compositions are provided for treating a urinary tract infection (UTI). The methods involve administering to a subject in need thereof a cAMP elevator or agent that mimics cAMP, particularly a labdane diterpene such as forskolin or a derivative or analog thereof in a therapeutically effective amount to treat a UTI. The methods may further include administration of at least one cAMP elevator in combination with one or more additional active compounds from other classes of therapeutic agents, such as antimicrobial agents or cholesterol lowering drugs. Compositions of the invention include pharmaceutical compositions and kits for treating a UTI in a subject in need thereof that include therapeutically effective amounts of at least two cAMP elevators, particularly where one of the cAMP elevators is a labdane diterpene such as forskolin or a derivative or analog thereof. In particular, the compositions and kits may also include at least one cAMP elevator in combination with one or more additional active compounds from other classes of therapeutic agents, such as antimicrobial agents or cholesterol lowering drugs.

The present invention provides methods and compositions for the consistent and quantitative differentiation of human preadipocytes isolated from adipose tissue into adipocytes bearing biochemical, genetic, and physiological characteristics similar to that observed in isolated primary adipocytes. The methods of the invention comprise incubating isolated human preadipocytes, plated at least about 25,000 cells / cm2, in a medium containing, glucose, a cyclic AMP inducer such as isobutylmethylxanthine or forskolin, a glucocorticoid or glucocorticoid analogue, insulin or an insulin analogue and a PPARγ agonist or a RXR agonist. The compositions of the invention include media for the differentiation of human preadipocytes, human adipocytes differentiated by the methods of the invention and transfected adipocytes. The present invention also provides methods for determining the ability of a compound to affect the differentiation of human preadipocytes to adipocytes, for determining the ability of a compound to act as a PPARγ antagonist. a glucocorticoid, a glucocoticoid analogue, or an insulin analogue, for transfecting cultured human adipocytes, and as a means to identify novel polypeptides secreted from human adipocytes into the conditioned medium. The methods and compositions have use in the drug discovery of compounds having relevance to the disease states of diabetes, obesity, and cardiovascular disease and in the studies of these diseases.

An administration method is provided, in which a composition comprising a forskolin 1α,9α-carbonate compound is administered to a human subject. According to an embodiment, the forskolin 1α,9α-carbonate compound has a skeletal structure of 8,13-epoxy-1α,6β,7β,9α-tetrahydroxylabd-14-en-11-one. A carbonyl group links the 1-position hydroxy oxygen and the 9-position hydroxy oxygen to one another for forming a carbonate ester ring. Hydrogen is appended to the 6-position hydroxy oxygen. A hydrogen or an acetyl group is appended to the 7-position hydroxy oxygen.

The invention relates to a method of inducing a human fibroblast to reprogram the human fibroblast into an osteoblast by utilization of Runx2 and a low-molecular-weight compound, particularly relates to a method of inducing a human fibroblast to transdifferentiate the human fibroblast into an osteoblast under the existence of dexamethasone by utilization of Runx2 gene expression, a low-molecular-weight compound CHIR99021 and / or a low-molecular-weight compound forskolin, and belongs to the fields of cytobiology and tissue engineering. The method includes: constructing a human skin fibroblast infected by a slow virus carrying Runx2-GFP, performing transdifferentiation of the human fibroblast under the existence of the dexamethasone by utilization of the low-molecular-weight compound CHIR99021 having a concentration of 5-10 muM and the low-molecular-weight compound forskolin having a concentration of 10 muM, changing into an osteoblast inducing liquid after 7-15 days, and inducing, and the fibroblast can be induced into the osteoblast after 5-20 days. The method can obtain osteoblasts simply and rapidly and can be used for cell therapy for bone metabolic disease, fracture, and the like. A pharmaceutical composition provided by the invention can be used for research, development and production of tissue-engineered bone, brings convenience to fundamental research and brings a prospect for clinical application.

Aqueous solutions of diterpenes such as Forskolin, its congeners, analogs and derivatives, up to approximately 6% concentration, are prepared using suitably substituted cyclodextrin as a solubilizing agents. In the absence of cyclodextrin, some diterpenes such as Forskolin are soluble in water only to concentrations of about 0.001%. Such aqueous solutions find applications in topical and systemic use, as pharmaceutical, cosmeceutical, nutraceutical preparations containing diterpenes such as Forskolin and congeners.

The invention discloses an induction medium inducing transdifferentiation of fibroblast into adipocyte, an induction method and application thereof. The induction medium contains a basal culture medium and an induction micromolecule combination, wherein the induction micromolecule combination is SG or 6TF, S is SB431542, G is GSK126, 6 is E61541, T is tranylcypromine, and F is forskolin. The induction medium can induce and trans-differentiate the fibrolast into the adipocyte, the obtained adipocyte contains a normal adipocyte specificity molecular tag and has a normal fat adipogenesis function, and a new approach is provided for solving the cellular source problem of regenerative medicine.

The present invention provides methods for reducing body weight. In particular, the present invention provides methods for reducing body weight by administering a composition comprising a forskolin 1α,9α-carbonate compound of the formula:where R1 is hydrogen or a carbonyl group.

Methods of activating a signaling cascade comprising, introducing leptin and / or a cytokine to a receptor complex comprising gp 130, optionally in combination with a compound acting on adenylate cyclase or acting on one or more downstream targets of adenylate cyclase, thereby inducing genes in neuro-endocrine cells or cells of neuro-endocrine origin. Two distinct gene-sets are induced, immediate early response genes (STAT-3, SOCS-3, Metallothionein-II, the serine / threonine kinase Fnk and the rat homologue of MRF-1), and late induced target genes (Pancreatitis Associated Protein I, Squalene Epoxidase, Uridinediphosphate Glucuronyl Transferase and Annexin VIII). Strong co-stimulation with the adenylate cyclase activator forskolin was shown with respect to late induced target genes. Transcripts encoding Leptin Induced Protein I (LIP-I) and Leptin Induced Protein II (LIP-II) were identified; however, no forskolin co-stimulatory effect was observed. It is also demonstrated that leptin modulates in vivo expression of MT-II, Fnk and Pancreatitis Associated Protein I genes.

The invention discloses an all-small molecular culture medium for culturing a liver organoid and an application of the all-small molecular culture medium. The culture medium comprises a basic culturemedium and a combination of small molecules, and the maintained combination of the small molecules is CBF, wherein C is CHIR-99021, B is Blebbistatin, C is Forskolin. The small molecules CHIR, Blebbistatin and Forskolin are added into the basic culture medium, so that the addition of a growth factor is replaced, a hpatic bile duct organoid can be cultured in vitro for a long time, and differentiation can be further induced to form a parenchymal hepatic cell. The method is beneficial to the in-vitro mass amplification of the liver organoid and provides the basis for researches and therapy of liver related diseases.

The invention relates to an isoforskolin preparing method. The method comprises the steps of utilizing forskolin as a raw material, utilizing a basic catalyst and a dichloromethane (DCM) solvent to carry out ethanoyl rearrangement reaction in an appropriate condition, filtering after reaction, separating liquid from solid, combining filter liquid, distilling the filter liquid to obtain a crude product and crystallizing and purifying the certain proportion and the certain amount of ethyl acetate (EA) and petroleum ether (PE) to prepare the high-purity isoforskolin with the purity larger than or equal to 99 percent.

The invention provides a composition used for transforming fibroblasts into PV (parvalbumin) neurons, also provides a method for transforming the fibroblasts into neuronal cells and further provides the neuronal cells prepared according to the method. The composition contains one or more of Ascl1 gene and FSK (forskolin). The invention further provides application of the composition and the neuronal cells to preparation of medicines for treating nervous system diseases. According to experiments, the PV neuronal cells can be efficiently obtained by means of transdifferentiation to treat epilepsy after transplantation, memory improvement can be realized by reducing frequency of epileptic seizures, and accordingly a new approach is created for treatment of epilepsy and related diseases.

The invention provides a method for reprogramming spinal marrow astrocytes into motor neurons through induction. The method comprises steps as follows: (1) primary rat astrocytes are subjected to pure culture; (2) 7 small molecule drugs including SB431542, LDN-193189, RA, bFGF, Purmorphamine, Forskolin and VPA are selected according to substances required in the stages of neuron induction and motor neuron formation and development, and the astrocytes are induced and reprogrammed in vitro through the small molecule drugs; (3) the reprogramming and differentiation conditions of the astrocytes to the motor neurons are analyzed through observation of morphologic change of cells and methods of chemical technology analysis of immunofluorescent cells, real-time fluorescent quantitative PCR analysis and statistical analysis. The rat astrocytes can be successfully induced and reprogrammed into the motor neutrons in vitro through small molecular drug composition, and the transdifferentiation exceeds 75%; in-situ direct reprogramming of the astrocytes to the neurons is a possibly comparatively feasible thought in SCI (spinal cord injury) repairing and functional reconstruction treatment.

The invention discloses a method for inducing transdifferentiation of fibroblasts to nerve cells. The method comprises the following steps: (1) culturing the fibroblasts for 20 to 30 hours; (2) transferring the fibroblasts into a culture medium containing an inducing micromolecular combination 6TCF, continuing to carry out culturing for 6 to 8 days, and replacing the culture medium once every 2 to 4 days during the culturing; (3) then, transferring the fibroblasts into a culture medium containing inducing micromolecular combinations 6TCF and 8CFV, continuing to carry out culturing for 7 to 16 days, and replacing the culture medium once every 2 to 4 days during the culturing, thereby obtaining the nerve cells, wherein 6 means E61541, T means tranylcypromine, C means CHIR99021, F means forskolin, 8 means A-83-01 and V means valproic acid. According to the method, through adding the inducing micromolecular combinations into the culture media, the fibroblasts can be trans-differentiated into the nerve cells through inducing, and the obtained nerve cells have specific molecular tags of normal nerve cells and have functions of the normal nerve cells, so that a new way is provided for solving the problem in cell sources of regenerative medicine.

A dermatological or cosmetological composition for an external topical administration, included together with pharmaceutically and / or cosmetologically acceptable excipients: at least one UVA-stabilizing and / or UVB-stabilizing screening agent, at least one compound capable of activating the endogenous synthesis of Heat Shock Protein (HSP) 32 or a functional peptide fragment of such a protein, and forskolin or any extract containing it.

The invention relates to stem cell differentiation technology in the technical field of stem cell treatment and in particular relates to a method for inducing differentiation of neural stem cells (NSCs) into dopaminergic neurons. The method is characterized by culturing 1-2 generation NSCs from the forebrain with a NSC basal culture medium until the diameters of neural spheres are 0.5-1mm, then changing the culture medium to an induction culture medium to enable the cells to grow adhering to the wall and obtaining dopaminergic neurons after culture for 3-10 days, wherein the induction culture medium contains inducers aFGF, TPA, forskolin, pramipexole and BMP-7. The method has the beneficial effects that after the NSCs from the forebrain are cultured by utilizing the induction culture medium, the proportion of the dopaminergic neurons obtained through differentiation of the NSCs is 30%, thus greatly increasing the differentiation rates of the dopaminergic neurons; the dopamine secretion rates of the neurons are increased by more than 20 times; the NSCs from the forebrain are effectively induced into the dopaminergic neurons.

A composition containing cAMP, cGMP, forskolin, adenylate cyclase or guanylate cyclase and microorganisms is provided to facilitate bioremediation, detoxication and to enhance plant growth in media contaminated with petroleum hydrocarbons. Methods to make the composition and apply it to the contaminated media in order to facilitate bioremediation and detoxication of such contaminants are also provided.

A nutritional supplement for increasing cognitive functioning. The supplement includes a flavonoid such as luteolin and a labdane diterpene such as forskolin. The supplement can also include one or any combination of L-phenylalanine, L-carnitine, acetyl-L-carnitine, and vitamin B6. Artichoke extract can be used as a source of luteolin. Methods of using the nutritional supplements to increase cognitive functioning are also included.