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.

The present disclosure provides compounds represented by Formula I: and the salts or solvates thereof, wherein R1, R3, L, Y, and B1 are as defined in the specification. Compounds having Formula I are SHP2 protein degraders useful for the treatment of cancer and other diseases.

The present disclosure provides compounds represented by Formula I: and the salts or solvates thereof, wherein R1, R3, L, Y, and B1 are as defined in the specification. Compounds having Formula I are SHP2 protein degraders useful for the treatment of cancer and other diseases.

The present disclosure provides a compound comprising a modified tetracycline derivative, covalently coupled through a linker defined by the generic formula XZX to a low-hydrophobicity bioactive molecule useful for treating neurodegenerative diseases, particularly a compound wherein the modified tetracycline derivative is a chemically modified doxycycline derivative and the low-hydrophobicity bioactive molecule useful for treating neurodegenerative diseases is dopamine. The disclosure also provides a process for preparing such compound, as well as methods for treating a neurodegenerative disease comprising administering said compound.

The present disclosure relates to a novel PLK1 degradation inducing compound, a method for preparing the same, and the use thereof. The compounds of the present disclosure exhibit an effect of inducing PLK1 degradation. Therefore, the compounds of the present disclosure may be effectively utilized for preventing or treating PLK1-related diseases.

The present disclosure relates to a novel PLK1 degradation inducing compound, a method for preparing the same, and the use thereof. The compounds of the present disclosure exhibit an effect of inducing PLK1 degradation. Therefore, the compounds of the present disclosure may be effectively utilized for preventing or treating PLK1-related diseases.

The present invention relates to conjugate compounds which comprise a peptide moiety (a) which is preferably a hydrophobic modified preS-derived peptide of hepatitis B virus or a respective cyclic peptide, and a NTCP substrate moiety (b), which is preferably a bile acid. The present invention further relates to pharmaceutical compositions comprising at least one conjugate compound. The present invention further relates to medical uses of said conjugate compounds and the pharmaceutical compositions, such as in the diagnosis, prevention and/or treatment of a liver disease or condition, and/or in the inhibition of HBV and/or HDV infection. The present invention further relates to methods of diagnosis, prevention and/or treatment of a said diseases and/or infections.

The present invention relates to a targeted protease degradation (TED) platform, and specifically to a conjugate of target molecule-linker-E3 ligase ligand as shown in formula I, R.sub.T-L1-R.sub.E3 (formula I), wherein R.sub.T is a monovalent group of the target molecule, R.sub.E3 is a monovalent group of the E3 ligase ligand, L1 is the linker linking A and B, and L1 is as shown in formula II below: —W-L2-W.sup.2— (II).

The present invention relates to a targeted protease degradation (TED) platform, and specifically to a conjugate of target molecule-linker-E3 ligase ligand as shown in formula I, R.sub.T-L1-R.sub.E3 (formula I), wherein R.sub.T is a monovalent group of the target molecule, R.sub.E3 is a monovalent group of the E3 ligase ligand, L1 is the linker linking A and B, and L1 is as shown in formula II below: —W-L2-W.sup.2— (II).

The present invention relates to bi-functional compounds which function to recruit endogenous proteins to an E3 ubiquitin ligase for degradation, and methods for using same. More specifically, the present disclosure provides specific proteolysis targeting chimera (PROTAC) molecules which find utility as modulators of targeted ubiquitination of a variety of polypeptides and other proteins, in particular the androgen receptor of a slice variant of AR which lacks the LBD, labelled as AR-V7, which are then degraded and/or otherwise inhibited by the compounds as described herein.