ERDs (Estrogen-Receptor Downregulators)

Page last modified on: July 2, 2008

At a Glance

ERDs keep estrogen from latching onto hormone receptors

Hormone receptors are like ears or antennae on a cell. Estrogen sends signals through the receptors that tell breast cancer cells to grow. Cells with estrogen receptors grow and multiply when estrogen attaches to the receptors. But ERDs like Faslodex break down those receptors so that estrogen can't latch on.

ERDs, or estrogen-receptor downregulators, block and break down estrogen receptors. With fewer hormone receptors available, fewer cancer cells receive the signal telling them to grow. This is how ERDs stop or slow down the growth of hormone-receptor-positive breast cancer cells.

The only ERD that's available is Faslodex (chemical name: fulvestrant). Faslodex is approved by the U.S. Food and Drug Administration (FDA) for post-menopausal women with hormone-receptor-positive metastatic breast cancer after other hormonal treatments, such as aromatase inhibitors or tamoxifen have stopped working.

Like SERMs (selective estrogen-receptor modulators, such as tamoxifen), ERDs bind to and block estrogen receptors so that estrogen cannot turn on the breast cancer cells. Tamoxifen and other SERMs block estrogen receptors in the breasts, but can act like weak estrogen in other parts of the body. Unlike SERMs, ERDs destroy estrogen receptors but do not act like weak estrogens anywhere else in the body.

ERDs do not seem to affect brain hormones, which stimulate the body's thermostat. For this reason, ERDs may cause fewer menopause-like side effects than tamoxifen, including hot flashes. ERDs are more like aromatase inhibitors in the degree and frequency of hot flashes and other menopausal symptoms, such as vaginal dryness and mood swings, they may cause.

  • Keep reading for specific information about Faslodex
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