Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in α-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in α-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

The present disclosure provides compounds of Formula (I-A) for inhibiting the interaction of menin with MLL1, MLL2 and MLL-fusion oncoproteins. The compounds are useful for the treatment of leukemia, solid cancers, diabetes and other diseases dependent on activity of MLL1, MLL2, MLL fusion proteins, and/or menin. ##STR00001##

The present disclosure provides compounds of Formula (I-A) for inhibiting the interaction of menin with MLL1, MLL2 and MLL-fusion oncoproteins. The compounds are useful for the treatment of leukemia, solid cancers, diabetes and other diseases dependent on activity of MLL1, MLL2, MLL fusion proteins, and/or menin. ##STR00001##

The present disclosure provides compounds of Formula (I-A) for inhibiting the interaction of menin with MLL1, MLL2 and MLL-fusion oncoproteins. The compounds are useful for the treatment of leukemia, solid cancers, diabetes and other diseases dependent on activity of MLL1, MLL2, MLL fusion proteins, and/or menin. ##STR00001##

A method of treating a subject for reducing the risk of QT space prolongation associated with the intake of a drug known to prolong QT space includes administering to the subject at least one specific inhibitor of mitochondrial ROS production selected from among anethole trithione (ATT), 4-OH-anethole trithione (ATX), and an ATX ester, and administering to the subject the drug known to prolong QT space.

A method of treating a subject for reducing the risk of QT space prolongation associated with the intake of a drug known to prolong QT space includes administering to the subject at least one specific inhibitor of mitochondrial ROS production selected from among anethole trithione (ATT), 4-OH-anethole trithione (ATX), and an ATX ester, and administering to the subject the drug known to prolong QT space.

Opioid-free, anesthetic, analgesic, antalgesic, anti-nociceptive, anti-inflammatory, antiemetic formulations, and methods for reducing pain, controlling pain, preventing pain, reducing or eliminating exposure to opioids, decreasing nausea and vomiting, featuring administration of the anesthetic/analgesic formulations. The opioid-free/sparing anesthetic/analgesic formulations comprise a local anesthetic, a cyclooxygenase (COX) inhibitor, and an alpha agonist. The formulations may optionally comprise additional compositions including but not limited to NMDA receptor antagonists, Buprenorphine, Dexketoprofen, Carprofen, an antifibrinolytic, an antibiotic, a steroid, a cyclooxygenase 3 inhibitor, a Transient Receptor Potential Vanilloid (TRPV) receptor agonist or antagonist, a protein kinase inhibitor, a competitive or non-competitive glycine or glutamate agonist, a glutamate or glycine inhibitor or antagonist, a neurokinin-1 receptor antagonist, an alpha agonist, a second alpha agonist, and combinations thereof. The formulations are effective for significantly reducing postoperative nausea and vomiting and enhancing postoperative pain relief as compared to existing prior art anesthetics/analgesics.

Opioid-free, anesthetic, analgesic, antalgesic, anti-nociceptive, anti-inflammatory, antiemetic formulations, and methods for reducing pain, controlling pain, preventing pain, reducing or eliminating exposure to opioids, decreasing nausea and vomiting, featuring administration of the anesthetic/analgesic formulations. The opioid-free/sparing anesthetic/analgesic formulations comprise a local anesthetic, a cyclooxygenase (COX) inhibitor, and an alpha agonist. The formulations may optionally comprise additional compositions including but not limited to NMDA receptor antagonists, Buprenorphine, Dexketoprofen, Carprofen, an antifibrinolytic, an antibiotic, a steroid, a cyclooxygenase 3 inhibitor, a Transient Receptor Potential Vanilloid (TRPV) receptor agonist or antagonist, a protein kinase inhibitor, a competitive or non-competitive glycine or glutamate agonist, a glutamate or glycine inhibitor or antagonist, a neurokinin-1 receptor antagonist, an alpha agonist, a second alpha agonist, and combinations thereof. The formulations are effective for significantly reducing postoperative nausea and vomiting and enhancing postoperative pain relief as compared to existing prior art anesthetics/analgesics.

Opioid-free, anesthetic, analgesic, antalgesic, anti-nociceptive, anti-inflammatory, antiemetic formulations, and methods for reducing pain, controlling pain, preventing pain, reducing or eliminating exposure to opioids, decreasing nausea and vomiting, featuring administration of the anesthetic/analgesic formulations. The opioid-free/sparing anesthetic/analgesic formulations comprise a local anesthetic, a cyclooxygenase (COX) inhibitor, and an alpha agonist. The formulations may optionally comprise additional compositions including but not limited to NMDA receptor antagonists, Buprenorphine, Dexketoprofen, Carprofen, an antifibrinolytic, an antibiotic, a steroid, a cyclooxygenase 3 inhibitor, a Transient Receptor Potential Vanilloid (TRPV) receptor agonist or antagonist, a protein kinase inhibitor, a competitive or non-competitive glycine or glutamate agonist, a glutamate or glycine inhibitor or antagonist, a neurokinin-1 receptor antagonist, an alpha agonist, a second alpha agonist, and combinations thereof. The formulations are effective for significantly reducing postoperative nausea and vomiting and enhancing postoperative pain relief as compared to existing prior art anesthetics/analgesics.