Abstract: A drive circuit includes a first drive unit, a second drive unit, and a third drive unit. The first drive unit is configured to: when receiving a first control signal, output a first drive charging current to a gate end, so that a voltage at the gate end reaches a first threshold. The second drive unit is configured to output a second drive charging current to the gate end, so that the voltage at the gate end reaches a second threshold from the first threshold. The third drive unit is configured to: after the voltage at the gate end reaches the second threshold, output a third drive charging current to the gate end. The third drive charging current is greater than the first drive charging current and the second drive charging current. In this way, a turn-on loss may be reduced while meeting an electromagnetic interference requirement of the power device.

Abstract: A conversion circuit and an adapter that resolve a voltage drop problem of a power supply of a driver in an ACF circuit. The conversion circuit includes an active clamp flyback circuit, a drive circuit, and a replenishment power transistor. The active clamp flyback circuit is configured to perform power conversion. The drive circuit is configured to output a drive signal and a reference voltage. The drive signal is used to drive the active clamp flyback circuit. A first terminal of the replenishment power transistor is coupled to an input terminal of the active clamp flyback circuit, a second terminal of the replenishment power transistor is coupled to a power supply terminal of the drive circuit, and a gate of the replenishment power transistor is configured to receive the reference voltage.

Abstract: A conversion circuit and an adapter that resolve a voltage drop problem of a power supply of a driver in an ACF circuit. The conversion circuit includes an active clamp flyback circuit, a drive circuit, and a replenishment power transistor. The active clamp flyback circuit is configured to perform power conversion. The drive circuit is configured to output a drive signal and a reference voltage. The drive signal is used to drive the active clamp flyback circuit. A first terminal of the replenishment power transistor is coupled to an input terminal of the active clamp flyback circuit, a second terminal of the replenishment power transistor is coupled to a power supply terminal of the drive circuit, and a gate of the replenishment power transistor is configured to receive the reference voltage.

Abstract: The subject invention relates to improved tocopheryl quinine derivatives and tocopherol derivatives having improved pharmacokinetics in vivo that can, in some embodiments, be useful in the treatment of Lysosomal Storage Disorder, restoration of normal mitochondrial ATP production, modulation of intracellular calcium ion concentration and other treatments or therapies. The tocopheryl quinone derivatives and tocopherol derivatives have side chains that have terminally halogenated carbon atoms.

Abstract: Disclosed are compounds of formula (I), formula (II), and formula (III): wherein Ar, R1, A, and X are as defined in the specification. These compounds are antiviral agents and are contemplated for use in the treatment of viral infections, for example, hepatitis C. These compounds are also contemplated for use in treating or preventing cancers.

Abstract: Disclosed are modulators of the human relaxin receptor 1, for example, of formula (I), wherein A, R1, and R2 are as defined herein, that are useful in treating mammalian relaxin receptor 1 mediated facets of human health, e.g., cardiovascular disease. Also disclosed is a composition comprising a pharmaceutically suitable carrier and at least one compound of the disclosure, and a method for therapeutic intervention in a facet of mammalian health that is mediated by a human relaxin receptor 1.

Abstract: The subject invention relates to improved tocopheryl quinine derivatives and tocopherol derivatives having improved pharmacokinetics in vivo that can, in some embodiments, be useful in the treatment of Lysosomal Storage Disorder, restoration of normal mitochondrial ATP production, modulation of intracellular calcium ion concentration and other treatments or therapies. The tocopheryl quinone derivatives and tocopherol derivatives have side chains that have terminally halogenated carbon atoms.

Abstract: The subject invention relates to improved tocopheryl quinone derivatives and tocopherol derivatives having improved pharmacokinetics in vivo that can, in some embodiments, be useful in the treatment of Lysosomal Storage Disorders, restoration of normal mitochondrial ATP production, modulation of intracellular calcium ion concentration and other treatments or therapies. The tocopheryl quinone derivatives and tocopherol derivatives have side chains that have terminally halogenated carbon atoms.

Abstract: Disclosed are modulators of the human relaxin receptor 1, for example, of formula (I), wherein A, R1, and R2 are as defined herein, that are useful in treating mammalian relaxin receptor 1 mediated facets of human health, e.g., cardiovascular disease. Also disclosed is a composition comprising a pharmaceutically suitable carrier and at least one compound of the disclosure, and a method for therapeutic intervention in a facet of mammalian health that is mediated by a human relaxin receptor 1.

Abstract: Disclosed are compounds of formula (I), formula (II), and formula (III): wherein Ar, R1, A, and X are as defined in the specification. These compounds are antiviral agents and are contemplated for use in the treatment of viral infections, for example, hepatitis C. These compounds are also contemplated for use in treating or preventing cancers.

Abstract: The disclosure includes compounds and pharmaceutically acceptable salts of Formula (I). Certain compounds and salts of Formula (I) are selective inhibitors of the Dopamine D2 receptor. The variables R1-R4, n, and L are defined herein. The disclosure also provides methods of synthesizing compounds of Formula (I) and pharmaceutical compositions containing compounds of Formula (I). Additionally the disclosure provides methods or treating patients suffering from central nervous system disorders, including Tourette's syndrome, bipolar disorder, hyperprolactinemia, tardive dyskinesia, Huntington's chorea, psychosis, depression, or schizophrenia.

Abstract: Disclosed are compounds of formula (I) (formula I), as antiviral agents, antineoplastic agents, pharmaceutical compositions comprising such compounds, and a method of use of these compounds, wherein X and Y are independently CH or N, o is 0, 1 or 2, and E is absent or is (CR13R14)m, NH, or S, F is absent or is (CR15R16)n, C=O, or —SO2—, G is absent or is (CR17 CR18)r, H is absent or is C?O, or —SO2- and R1, Ar1, Ar2 are as defined in the specification. These compounds are antiviral agents and are contemplated in the treatment of viral infections, for example, hepatitis C, or are antineoplastic agents.

Abstract: Disclosed are modulators of the human relaxin receptor 1, for example, of formula (I), wherein A, R1, and R2 are as defined herein, that are useful in treating mammalian relaxin receptor 1 mediated facets of human health, e.g., cardiovascular disease. Also disclosed is a composition comprising a pharmaceutically suitable carrier and at least one compound of the disclosure, and a method for therapeutic intervention in a facet of mammalian health that is mediated by a human relaxin receptor 1.

Abstract: The present invention provides a composition and related methods for delivering cargo to a mitochondria which includes (a) a membrane active peptidyl fragment having a high affinity with the mitochondria and (b) cargo. The cargo may be selected from a wide variety of desired cargos which are to be delivered to the mitochondria for a specific purpose. Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using the structural signaling of the ?-turn recognizable by cells as mitochondria) targeting sequences are discussed. Mitochondria and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient.

Abstract: The subject invention relates to improved tocopheryl quinone derivatives and tocopherol derivatives having improved pharmacokinetics in vivo that can, in some embodiments, be useful in the treatment of Lysosomal Storage Disorders, restoration of normal mitochondrial ATP production, modulation of intracellular calcium ion concentration and other treatments or therapies. The tocopheryl quinone derivatives and tocopherol derivatives have side chains that have terminally halogenated carbon atoms.

Abstract: The disclosure includes compounds and pharmaceutically acceptable salts of Formula (I). Certain compounds and salts of Formula (I) are selective inhibitors of the Dopamine D2 receptor. The variables R1-R4, n, and L are defined herein. The disclosure also provides methods of synthesizing compounds of Formula (I) and pharmaceutical compositions containing compounds of Formula (I). Additionally the disclosure provides methods or treating patients suffering from central nervous system disorders, including Tourette's syndrome, bipolar disorder, hyperprolactinemia, tardive dyskinesia, Huntington's chorea, psychosis, depression, or schizophrenia.

Abstract: The present invention provides a composition and related methods for delivering cargo to a mitochondria which includes (a) a membrane active peptidyl fragment having a high affinity with the mitochondria and (b) cargo. The cargo may be selected from a wide variety of desired cargos which are to be delivered to the mitochondria for a specific purpose. Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using the structural signaling of the ?-turn recognizable by cells as mitochondria) targeting sequences are discussed. Mitochondria and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient.

Abstract: Disclosed are modulators of the human relaxin receptor 1, for example, of formula (I), wherein A, R1, and R2 are as defined herein, that are useful in treating mammalian relaxin receptor 1 mediated facets of human health, e.g., cardiovascular disease. Also disclosed is a composition comprising a pharmaceutically suitable carrier and at least one compound of the disclosure, and a method for therapeutic intervention in a facet of mammalian health that is mediated by a human relaxin receptor 1.

Abstract: The present invention provides a composition and related methods for delivering cargo to a mitochondria which includes (a) a membrane active peptidyl fragment having a high affinity with the mitochondria and (b) cargo. The cargo may be selected from a wide variety of desired cargoes which are to be delivered to the mitochondria for a specific purpose. Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using the structural signaling of the ?-turn recognizable by cells as mitochondria) targeting sequences are discussed. Mitochondria and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient.

Abstract: The present invention provides a composition and related methods for delivering cargo to a mitochondria which includes (a) a membrane active peptidyl fragment having a high affinity with the mitochondria and (b) cargo. The cargo may be selected from a wide variety of desired cargoes which are to be delivered to the mitochondria for a specific purpose. Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using the structural signaling of the ?-turn recognizable by cells as mitochondria) targeting sequences are discussed. Mitochondria and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient.