breast cancer drugs

American researchers recently developed a new class of molecules that may improve breast cancer treatment.

Tens of millions of women suffer from breast cancer worldwide. More than 70% of breast cancers are “ER-positive,” meaning that the cancer cells grow in response to estrogen. In order to treat this type of breast cancer, doctors use endocrine therapy to break down estrogen receptors in the cancer cells.

Small molecules called selective estrogen receptor degraders (SERDs), target and damage cancer cells’ estrogen receptors. This type of therapy is often the last line of treatment for patients with resistant or metastatic breast cancer. Currently, there is only one SERD approved by the FDA and the delivery of the drug requires painful injections. So, researchers are looking for new small molecules that can block cancer cell growth and degrade estrogen receptors in breast cancers.

A team of researchers from the United States developed a new class of SERD molecules that have a great potential to stop breast cancer tumor growth. These molecules have a unique structure that was only recently discovered to hinder estrogen receptors. The research was published in ACS Medicinal Chemistry Letters.

The structure and modular design of the new molecules allowed the researchers to make different variations SERDs with relative ease. Then, they tested 15 of these molecules on breast cancer cells. Experiments proved that the estrogen receptors in the cells were damaged and the growth of breast cancer cells slowed when treated with the novel molecules.

This research greatly increases the number of options for ER-positive breast cancer treatment. In the future, researchers plan to test a few of the most promising molecules in mice to develop them into new breast cancer drugs.

Written by Cindi A. Hoover, Ph.D.

References: Wang L, Guillen VS, Sharma N et al. New class of selective estrogen receptor degraders (SERDs): Expanding the toolbox of PROTAC degrons. 2018. ACS Med Chem Lett. 9:803-808. https://www.eurekalert.org/pub_releases/2018-10/siot-anm100318.php

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