Table 3.

Approaches to treating bone metastases [147–149].

Therapy	Mechanism	Stage of clinical development
Bisphosphonates	Block bone resorption; might block tumour-cell mitosis and stimulate tumour-cell apoptosis; alleviate bone pain	On the market
Denosumab	A human antibody that is effective in preventing bone loss and bone deterioration	On the market
Targeted therapy
(a) Monoclonal antibodies (palbocilib, ribociclib, and abemaciclib)	Trigger an immune system response that can destroy the outer wall of a cancer cell	On the market
(b) With HER2 negative breast cancer (olaparib and talazoparib)	Trap the PARP-1 protein at a single-stranded break and disrupt its catalytic cycle, leading to replication fork progression and double-strand breaks	Phase III
(c) With metastatic breast cancer (trastuzumab deruxtecan)	Inhibits HER2 homodimerization, thereby preventing HER2-mediated signalling	Phase III
Osteoprotegerin	Prevents RANKL from binding its receptor and stimulating osteoclasts	Phase II
RANK-Fc	Prevents RANKL from binding its receptor and stimulating osteoclasts	Phase I
PTHrP antibodies	Neutralize PTHrP	Phase III
Vitamin D analogues	Decrease PTHrP production	Phase III
Hormonal therapy (tamoxifen, anastrozole, exemestane, letrozole, gasorelin, fulvestrant, and elacestrant)	Restore the balance between bone resorption and formation, slowing bone loss and increasing bone mass	On the market (generic)

Abbreviations: PTHrP, parathyroid-hormone-related peptide; RANK, receptor activator of nuclear factor-κB; RANKL, receptor activator of nuclear factor-κB ligand.