SERDs function by binding to the estrogen receptor, changing its shape, and marking it for degradation through the ubiquitin-proteasome pathway. This process leads to the receptor's destruction, preventing it from activating genes that promote cell proliferation. Unlike selective estrogen receptor modulators (SERMs), which block the receptor's activity but do not degrade it, SERDs offer a more robust approach to inhibiting estrogen-driven cancer growth.
