The present invention provides compositions and methods for the treatment of neoplasms, in particular, by targeting of quiescent and proliferating cancers cells with DYRK1 inhibitor in combination with other treatments effective against certain neoplastic conditions, in particular, anti-cancer treatment with a MEK inhibitor or a b-RAF inhibitor, or a KRAS inhibitor.

The present disclosure relates to recombinant EGFL7, EGFL7 antibodies, and uses thereof.

The present disclosure relates to recombinant EGFL7, EGFL7 antibodies, and uses thereof.

The invention relates to selective small molecule human constitutive androstane receptor (hCAR) activators of Formula (I) or (II), pharmaceutical compositions thereof, and use thereof for the treatment of hematologic malignancies and other cancers. The small molecule hCAR activator in combination with CPA based chemotherapy regimen provides a synergistic effect to help promote cytoxicity of the cyclophosphamide (CPA) based anticancer treatments including CHOP regimen (CPA, doxorubicin, vincristine, and prednisone) by preferential induction of CYP2B6 over CYP3A4 and promoting the formation of therapeutically active CPA metabolite 4-OH-CPA.

The invention relates to selective small molecule human constitutive androstane receptor (hCAR) activators of Formula (I) or (II), pharmaceutical compositions thereof, and use thereof for the treatment of hematologic malignancies and other cancers. The small molecule hCAR activator in combination with CPA based chemotherapy regimen provides a synergistic effect to help promote cytoxicity of the cyclophosphamide (CPA) based anticancer treatments including CHOP regimen (CPA, doxorubicin, vincristine, and prednisone) by preferential induction of CYP2B6 over CYP3A4 and promoting the formation of therapeutically active CPA metabolite 4-OH-CPA.

The present invention provides methods for improving or accelerating wound healing in a subject comprising administering to a wound of the subject in need thereof an agent that suppresses expression of a clock gene, wherein the clock gene is neuronal PAS domain protein 2 (Npas2). This invention also relates to methods for regenerating alveolar bone, regenerating connective tissue at a wound site, and for decreasing wound area size comprising administering to a bone loss site or a wound site, in particular, an open wound site, of a subject an agent that suppresses expression of Npas2.

Disclosed herein are compositions and methods for an embolizing agent precursor. The embolizing agent precursor may include a gaseous component and a first stabilizer to stabilize the gaseous component, the first stabilizer may include a a polymer, and wherein a gas portion of the gaseous component is selected from the group consisting of sulphur hexafluoride and C3-6 perfluorocarbons. The embolizing agent precursor may further include an oil component which comprises a C1-7 hydrocarbon, a second stabilizer to stabilize the oil component, and a vaporous component configured to enlarge the gaseous component.

Disclosed herein are compositions and methods for an embolizing agent precursor. The embolizing agent precursor may include a gaseous component and a first stabilizer to stabilize the gaseous component, the first stabilizer may include a a polymer, and wherein a gas portion of the gaseous component is selected from the group consisting of sulphur hexafluoride and C3-6 perfluorocarbons. The embolizing agent precursor may further include an oil component which comprises a C1-7 hydrocarbon, a second stabilizer to stabilize the oil component, and a vaporous component configured to enlarge the gaseous component.

The invention provides compositions comprising a single protein having one or more molecules of a pharmaceutical agent tightly bound therein. The compositions are useful to decrease the toxicity and/or to widen the therapeutic window of the pharmaceutical agent. The invention also provides methods for preparing such a composition.

Disclosed are methods for treating specific genetic subtypes of diffuse large B cell lymphoma using a combination of a BTK inhibitor and R-CHOP chemotherapy. The methods produce favorable event-free survival and overall survival rates among subjects exhibiting the genetic subtypes.