The present disclosure relates to a medicament for treating cholangiocarcinoma with KRAS mutations. Specifically, the present invention relates to a method of ER inhibitors for the specific treatment of cholangiocarcinoma with KRAS mutations, and to a use of ER inhibitors in the preparation of a medicament for the treatment of cholangiocarcinoma with KRAS mutations. New therapeutic regimens for patients suffering from cholangiocarcinoma with KRAS mutations are provided to improve the possibility of therapeutic benefit for patients.

Disclosed herein are methods of treating a subject with an estrogen receptor-positive (ER+) breast cancer comprising obtaining a sample of the breast cancer from the subject; determining a level of E-cadherin in the sample is reduced compared to a control; and administering a therapeutically effective amount of an IGF1R pathway inhibitor and an endocrine therapeutic. Also disclosed herein are methods to treat a cancer in a subject comprising administering a therapeutically effective amount of an IGF1R pathway inhibitor and an E-cadherin inhibitor. Also disclosed are methods to predict the likelihood a subject with a breast cancer will respond therapeutically to a treatment comprising administering an IGF1R pathway inhibitor, the method comprising obtaining a sample of the cancer from the subject; and determining a level of E-cadherin in the sample.

Disclosed herein are methods of treating a subject with an estrogen receptor-positive (ER+) breast cancer comprising obtaining a sample of the breast cancer from the subject; determining a level of E-cadherin in the sample is reduced compared to a control; and administering a therapeutically effective amount of an IGF1R pathway inhibitor and an endocrine therapeutic. Also disclosed herein are methods to treat a cancer in a subject comprising administering a therapeutically effective amount of an IGF1R pathway inhibitor and an E-cadherin inhibitor. Also disclosed are methods to predict the likelihood a subject with a breast cancer will respond therapeutically to a treatment comprising administering an IGF1R pathway inhibitor, the method comprising obtaining a sample of the cancer from the subject; and determining a level of E-cadherin in the sample.

A dermal skin protectant and carrier comprising a combination of two different viscosity dimethicone components, wherein the difference between the two different viscosity dimethicone components is about 2.0 million cP or greater; and comprising at least one active ingredient.

A dermal skin protectant and carrier comprising a combination of two different viscosity dimethicone components, wherein the difference between the two different viscosity dimethicone components is about 2.0 million cP or greater; and comprising at least one active ingredient.

This invention relates to methods of using salt inducible kinase inhibitors to enhance female fertility.

This invention relates to methods of using salt inducible kinase inhibitors to enhance female fertility.

The disclosure provides methods and compositions for treating heart conditions. In particular, the disclosure provides compositions comprising lithium, or a salt thereof, either alone or in combination with at least one additional anti-arrhythmia agent, and methods for treating heart conditions using such compositions.

The disclosure provides methods and compositions for treating heart conditions. In particular, the disclosure provides compositions comprising lithium, or a salt thereof, either alone or in combination with at least one additional anti-arrhythmia agent, and methods for treating heart conditions using such compositions.

It is proposed that dissipation of relative benefit during long-term treatment is due to long-term tolerance to stimulant medications. To improve adherence and persistence of medication use, it is advantageous to develop medications that are not undermined by long-term tolerance. Disclosed herein in certain implementations are formulations and methods relating to an alternative formulation of medication for the treatment of ADHD based on two principles: (a) retaining the initial immediate-release component of controlled-release formulations that targets a neural mechanism, which elicits acute tolerance, and (b) replacing the subsequent sustained-release component with a medication that maintains the initial benefit by targeting a different neural mechanism does not elicit tolerance, thus allowing more time for acute tolerance elicited by the initial bolus dose of stimulant medication to dissipate completely each day and avoid carry-over and accumulation that results in long-term tolerance.