A method for treating and/or preventing VacA+ H. pylori infection and a disorder associated with VacA+ H. pylori infection is provided. The method comprises the administration of TRPML agonists such as ML-SA1, SF-22, SF-51, MK6-83 and their derivatives.

A method for treating and/or preventing VacA+ H. pylori infection and a disorder associated with VacA+ H. pylori infection is provided. The method comprises the administration of TRPML agonists such as ML-SA1, SF-22, SF-51, MK6-83 and their derivatives.

Disclosed herein, inter alia, are compositions and methods for targeting E3 ligases. In an aspect is a targeted protein degrader including 1) a targeted protein binder and 2) an E3 Ubiquitin ligase binder, wherein the E3 Ubiquitin ligase is human RNF4 or human RNF114. In an aspect is provided a pharmaceutical composition including a compound as described herein, including embodiments, and a pharmaceutically acceptable excipient.

Disclosed herein, inter alia, are compositions and methods for targeting E3 ligases. In an aspect is a targeted protein degrader including 1) a targeted protein binder and 2) an E3 Ubiquitin ligase binder, wherein the E3 Ubiquitin ligase is human RNF4 or human RNF114. In an aspect is provided a pharmaceutical composition including a compound as described herein, including embodiments, and a pharmaceutically acceptable excipient.

Methods and compositions for potentiating the effect of an opioid analgesic in a patient undergoing or planning to undergo opioid analgesic therapy using a potentiating amount of iboga alkaloid or pharmaceutically acceptable salt and/or solvate thereof that does not prolong the patient's QT interval by more than about 50 milliseconds.

Methods and compositions for potentiating the effect of an opioid analgesic in a patient undergoing or planning to undergo opioid analgesic therapy using a potentiating amount of iboga alkaloid or pharmaceutically acceptable salt and/or solvate thereof that does not prolong the patient's QT interval by more than about 50 milliseconds.

Methods and compositions for potentiating the effect of an opioid analgesic in a patient undergoing or planning to undergo opioid analgesic therapy using a potentiating amount of iboga alkaloid or pharmaceutically acceptable salt and/or solvate thereof that does not prolong the patient's QT interval by more than about 50 milliseconds.

The present invention relates to a delivery contact lens device for delivering cargo molecules. The device comprises cargo molecules and a nanocomposite comprising hydrophilic polymer domains, hydrophobic polymer domains, aqueous pores, and charged boundary double layers, wherein at least 80% of the cargo molecule partitions in the charged boundary double layers formed at the interface of (i) aqueous pores and (ii) either hydrophobic polymer domains or hydrophilic polymer domains, the charged boundary double layers have a surface charge density of 0.005 to 0.5 Coulomb/meter.sup.2, and the aqueous pores including the cargo molecules have a low ionic strength of 0.1 to 100 mM, and osmolarity of 200-300 mM. The device retains the cargo molecules within the contact lens in a storage mode under a low ionic strength condition and releases the cargo molecules immediately after being placed in a tear environment with a higher ionic strength through the ion exchange process with the tear film, for triggering a spontaneous release, slowing down the burst release as well as precisely controlling the release kinetics.

The present invention relates to a delivery contact lens device for delivering cargo molecules. The device comprises cargo molecules and a nanocomposite comprising hydrophilic polymer domains, hydrophobic polymer domains, aqueous pores, and charged boundary double layers, wherein at least 80% of the cargo molecule partitions in the charged boundary double layers formed at the interface of (i) aqueous pores and (ii) either hydrophobic polymer domains or hydrophilic polymer domains, the charged boundary double layers have a surface charge density of 0.005 to 0.5 Coulomb/meter.sup.2, and the aqueous pores including the cargo molecules have a low ionic strength of 0.1 to 100 mM, and osmolarity of 200-300 mM. The device retains the cargo molecules within the contact lens in a storage mode under a low ionic strength condition and releases the cargo molecules immediately after being placed in a tear environment with a higher ionic strength through the ion exchange process with the tear film, for triggering a spontaneous release, slowing down the burst release as well as precisely controlling the release kinetics.

The invention relates to the use of a mGluR5 antagonist for the treatment of opioid analgesic tolerance associated with chronic opioid use in chronic pain.