Bone & Mineral Metabolism Research Reagents

Bone is a dynamic tissue maintained by continuous remodeling — the balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Disruption of this balance causes osteoporosis, Paget’s disease, and cancer-associated bone destruction. The RANKL/OPG axis is the central regulatory mechanism of osteoclastogenesis, targeted by denosumab (anti-RANKL); the WNT/Sclerostin pathway controls osteoblast activity, targeted by romosozumab (anti-Sclerostin). Parathyroid hormone (PTH) integrates calcium homeostasis with bone turnover. Studying these pathways requires well-characterized recombinant proteins for functional assays and validated antibodies for pathway activation readouts.

Research Use Only (RUO)Not intended for diagnostic or therapeutic procedures.

abinScience provides validated antibodies, recombinant proteins, and ELISA kits for key bone and mineral metabolism targets — osteoclast regulators, osteoblast mediators, and bone turnover markers. All products are manufactured by our parent company AtaGenix Laboratories under ISO quality systems. Browse products below or contact us for custom development.

Osteoclast Regulation & Bone Resorption

RANKL (TNFSF11 / TRANCE / ODF) — Receptor activator of NF-κB ligand is the essential cytokine for osteoclast differentiation, activation, and survival. RANKL binds RANK on osteoclast precursors to drive multinucleated osteoclast formation via NF-κB and NFATc1 signaling. Denosumab (anti-RANKL monoclonal antibody) is a first-line therapy for osteoporosis and bone metastases. Recombinant RANKL proteins are widely used for in vitro osteoclastogenesis assays and drug screening.
→ Browse RANKL antibodies & proteins

OPG (Osteoprotegerin / TNFRSF11B) — Soluble decoy receptor for RANKL that blocks osteoclast differentiation by preventing RANKL-RANK interaction. The RANKL/OPG ratio determines net bone resorption activity and is a key readout in bone biology research. OPG deficiency causes juvenile Paget’s disease with severe osteopenia.
→ Browse OPG antibodies & proteins

Cathepsin K (CTSK) — The dominant cysteine protease secreted by osteoclasts into the resorption lacuna, responsible for degrading type I collagen in bone matrix. Cathepsin K inhibitors (odanacatib) were developed as anti-resorptive agents. Anti-Cathepsin K antibodies serve as osteoclast activity markers in IHC and functional assays.
→ Browse Cathepsin K antibodies & proteins

Osteoblast Regulation & Bone Formation

Sclerostin (SOST) — A glycoprotein secreted by osteocytes that inhibits WNT/β-Catenin signaling in osteoblasts, suppressing bone formation. Loss-of-function mutations in SOST cause sclerosteosis (high bone mass). Romosozumab (anti-Sclerostin monoclonal antibody) is the first bone-forming biologic approved for osteoporosis, stimulating osteoblast activity while reducing resorption. Recombinant Sclerostin proteins support WNT pathway inhibition studies and drug screening assays.
→ Browse Sclerostin antibodies & proteins

Osteocalcin (BGLAP / Bone Gla Protein) — The most abundant non-collagenous protein in bone matrix, secreted by osteoblasts during mineralization. Serum osteocalcin is a clinical bone formation marker used to monitor osteoporosis treatment response. Undercarboxylated osteocalcin also functions as a hormone regulating glucose metabolism and male fertility, linking bone to metabolic endocrinology.
→ Browse Osteocalcin antibodies & proteins

Calcium & Phosphate Homeostasis

PTH (Parathyroid Hormone) — An 84-amino-acid peptide secreted by the parathyroid glands in response to low serum calcium. PTH raises calcium by stimulating osteoclastic bone resorption, renal calcium reabsorption, and 1,25(OH)₂D synthesis. Intermittent low-dose PTH (teriparatide) paradoxically stimulates bone formation and is used as an anabolic therapy for severe osteoporosis. PTH immunoassays must distinguish intact PTH(1-84) from inactive C-terminal fragments that accumulate in renal failure.
→ Browse PTH antibodies & proteins

Vitamin D Receptor (VDR) / CYP27B1 — VDR is a nuclear receptor that mediates the genomic actions of 1,25-dihydroxyvitamin D (calcitriol) on calcium absorption, bone mineralization, and immune modulation. CYP27B1 (1α-hydroxylase) catalyzes the final activation step of vitamin D in the kidney. VDR polymorphisms are associated with osteoporosis susceptibility and fracture risk.
→ Browse Vitamin D Receptor antibodies & proteins

References

1. Boyle WJ, et al. Osteoclast differentiation and activation. Nature. 2003;423(6937):337-342. DOI

2. Cosman F, et al. Romosozumab treatment in postmenopausal women with osteoporosis. N Engl J Med. 2016;375(16):1532-1543. DOI

3. Cummings SR, et al. Denosumab for prevention of fractures in postmenopausal women with osteoporosis. N Engl J Med. 2009;361(8):756-765. DOI

4. Lee NK, et al. Endocrine regulation of energy metabolism by the skeleton. Cell. 2007;130(3):456-469. DOI