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This technology includes the compositions and methods for inhibiting PIN1 for the treatment of disorders characterized by elevated PIN1 levels (e.g., immune disorders, proliferative disorders, and neurodegenerative disorders) with small molecules. Pin1 dysregulation has been associated with a number of pathological conditions. In particular, PIN1 has been shown to promote oncogenesis by modulating several oncogenic signaling pathways and its overexpression has been shown to correlate with poor clinical outcome.

This technology includes a stable pharmaceutical formulation of propofol hemisuccinate for inhalation delivery to treat intractable epilepsy and migraine. The formulation can be used to treat a patient experiencing a seizure aura to prevent a motor seizure. Alternatively, the formulation can be used to treat an epileptic patient who is experiencing seizure clusters in an out-of-hospital or in-hospital setting. For migraines, the formulation can be used to treat a patient experiencing a migraine aura or early migraine to forestall the development of the full symptoms of a migraine headache.

This technology includes a series of imidazo[1,2-b]pyridazines that display potent inhibition of FLT3, as well as potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against the common clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML.

This technology includes a series of imidazo[1,2-b]pyridazines that display potent inhibition of FLT3, as well as potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against the common clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML.

This technology includes a series of imidazo[1,2-a]pyridines with potent inhibition of FLT3, which retains potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against the common clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML. This invention builds upon an earlier IP position with new analogs.

This technology includes a series of imidazo[1,2-a]pyrazines that display potent inhibition of FLT3, as well as potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against the common clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML.

This technology includes a series of imidazo[1,2-a]pyridines with potent inhibition of FLT3, which retains potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against the common clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML. This invention builds upon an earlier IP position with new analogs.

This technology includes a series of diphenylpropanamides as potent and selective RORgt inhibitors for the treatment of Th17-related autoimmune diseases. The retinoic acid-related orphan receptor RORgt plays an important role in the differentiation of thymocytes, lymphoid tissue inducer cells, and inflammatory T helper-expressing interleukin 17a (Th17) cells. Small molecule RORgt inhibitors may provide means to regulate Th17 mediated immune response. The novel molecules have potential to treat Th17-related autoimmune diseases.

This technology includes two new salt forms for (2R,6R)-hydroxynorketamine (2R,6R-HNK), which is the lead molecule being developed for treatment-resistant depression. Currently, 2R,6R-HNK is being developed as the HCl salt. The HCl salt is slightly hygroscopic at high RH. This is a potential liability, especially in an oral pill form. Recently the malonate and salicylate salt have been discovered and found to have excellent crystalline behavior while also not having the hygroscopic liability the HCl salt holds. This represents a clear advantage.

This technology includes a series of diphenylpropanamides as potent and selective RORgt inhibitors for the treatment of Th17-related autoimmune diseases. The retinoic acid-related orphan receptor RORgt plays an important role in the differentiation of thymocytes, lymphoid tissue inducer cells, and inflammatory T helper-expressing interleukin 17a (Th17) cells. Small molecule RORgt inhibitors may provide means to regulate Th17 mediated immune response.