Among other things, the present disclosure provides compounds, compositions thereof, and methods of using the same. In some embodiments, compounds of the present disclosure bind to Fc receptors, e.g., CD16a. In some embodiments, compounds of the present disclosure are useful for treating various conditions, disorders or diseases including cancer.

This disclosure provides a dosage regimen for co-administration of enzalutamide and a strong CYP3A4 inducer.

This disclosure provides a dosage regimen for co-administration of enzalutamide and a strong CYP3A4 inducer.

This disclosure provides a dosage regimen for co-administration of enzalutamide and a strong CYP3A4 inducer.

The invention includes 2-β-naphthyl-acetic acid derivatives, which are selective AKR1C3 inhibitors. In certain embodiments, the compounds of the invention are R-naproxen analogs. The invention further includes methods of treating cancer, such as prostate cancer and/or castration-resistant prostate cancer, using at least one compound of the invention.

Among other things, the present disclosure provides compounds, compositions thereof, and methods of using the same. In some embodiments, compounds of the present disclosure bind to Fc receptors, e.g., CD16a. In some embodiments, compounds of the present disclosure are useful for treating various conditions, disorders or diseases including cancer.

Disclosed herein are bicyclic pyridines, such as thienopyridine, pyrrolopyridine, furopyridine compounds, and methods for treating cancers.

Disclosed herein are bicyclic pyridines, such as thienopyridine, pyrrolopyridine, furopyridine compounds, and methods for treating cancers.

Disclosed here in are methods and kits for identifying a prostate cancer treatment for a subject. The methods include obtaining a fluid sample from the subject, the fluid sample comprising noncellular DNA (ncDNA) from the subject, transforming the ncDNA into a plurality of genomic variations to determine if the ncDNA contains castration-resistant structural variations including at least one of a genomic alteration in AR encoding an androgen receptor and a genomic alteration of an AR enhancer; and identifying the prostate cancer treatment for the subject based on the plurality of genomic variations.

Disclosed herein are Ral-antagonist compounds that covalently bind to binding sites in RalA, and efficaciously inhibit Ral activity. The compounds include aryl sulfonyl fluoride compounds of the general structure of wherein X and Y are independently C or N, and R.sub.4 is C.sub.1-C.sub.4 alkyl, —OCH.sub.3, —OCH.sub.2CH.sub.3, —OCH(CH.sub.3).sub.2, —(SO.sub.2)CH.sub.3, —OH, or halo. These compounds expand Ral-inhibiting therapeutic options for treating Ral-driven cancers and one embodiment of the present disclosure is directed to the use of such compounds to treat cancer.