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RANKL/OPG

" in MedChemExpress (MCE) Product Catalog:

By Targets:	RANKL/RANK (5) Apoptosis (1) ERK (2) Interleukin Related (2) MAP3K (2) MEK (2) MMP (1) NF-κB (2) NOD-like Receptor (NLR) (2) Nuclear Factor of activated T Cells (NFAT) (1) p38 MAPK (2) PPAR (1) Reference Standards (1) SARS-CoV (2) Toll-like Receptor (TLR) (2) Wnt (3) β-catenin (3)
By Research Areas:	Cancer (3) Infection (2) Inflammation/Immunology (7) Metabolic Disease (4)

9

Inhibitors & Agonists

2

Peptides

3

Natural
Products

Targets Recommended: RANKL/RANK

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

Boldine 1 Publications Verification	RANKL/RANK Apoptosis	Inflammation/Immunology Cancer
Boldine is an apomorphine isoquinoline alkaloid extracted from the root of the pheasant pepper (Litsea cubeba). Boldine is an oral effective antioxidant, anti-inflammatory, antitumor agent, and can inhibit osteoclast formation. Boldine induces apoptosis of human bladder cancer cells by regulating ERK, AKT and GSK-3β. Boldine ameliorates bone destruction by down-regulating the *OPG/RANKL/RANK* signaling pathway. It can be used in rheumatoid arthritis research .

Pamidronic acid 1 Publications Verification	RANKL/RANK Toll-like Receptor (TLR) Wnt β-catenin	Metabolic Disease Inflammation/Immunology Cancer
Pamidronic acid, the second-generation nitrogen-containing bisphosphonate, is an inhibitor of bone loss. Pamidronic acid significantly inhibits subchondral bone loss in early osteoarthritis by upregulating the expression of *OPG* in cartilage and subchondral bone, and inhibiting the expression of *RANKL* and MMP-9 in both tissues, as well as TLR-4 in cartilage, thereby alleviating cartilage degeneration. Additionally, Pamidronic acid can inhibit the signaling of Wnt and β-catenin, and is applicable for research on osteoporosis and osteosarcoma .

TriDAP dihydrochloride 1 Publications Verification L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride	NOD-like Receptor (NLR) NF-κB MAP3K MEK ERK p38 MAPK Interleukin Related SARS-CoV	Infection Inflammation/Immunology
TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a K_d value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the *RANKL/OPG* ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection .

Boldine (Standard) 1 Publications Verification	Reference Standards RANKL/RANK	Inflammation/Immunology
Boldine (Standard) is the analytical standard of Boldine. This product is intended for research and analytical applications. Boldine is an aporphine isoquinoline alkaloid extracted from the root of Litsea cubeba and also possesses these properties, including antioxidant, anti-inflammatory and cytoprotective effects. Boldine suppresses osteoclastogenesis, improves bone destruction by down-regulating the *OPG/RANKL/RANK* signal pathway and may be a potential therapeutic agent for rheumatoid arthritis .

E0924G	PPAR	Metabolic Disease
E0924G is an orally active activator for PPARδ with EC₅₀ of 2.82 μM. E0924G promotes the upregulation of osteoprotegerin (OPG) with an EC₅₀ of 0.29 μM. E0924G reduces RANKL-induced osteoclast differentiation and inhibites F-actin ring formation in RAW264.7 macrophages. E0924G regulates the bone density and bone loss in ovariectomized (OVX) and age-related osteoporosis models .

TriDAP L-Ala-γ-D-Glu-meso-diaminopimelic acid	NOD-like Receptor (NLR) NF-κB MAP3K MEK ERK p38 MAPK Interleukin Related SARS-CoV	Infection Inflammation/Immunology
TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a NOD1 agonist with a K_d value of 34.5 μM. TriDAP enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP decreases IκBα levels and increases p65 levels. TriDAP induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP increases the *RANKL/OPG* ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection .

Phlorigidoside C	Others	Inflammation/Immunology
Phlorigidoside C, a natural iridoid glucoside, possesses anti-rheumatoid arthritis effect .

Pamidronic acid (Standard)	RANKL/RANK Toll-like Receptor (TLR) Wnt β-catenin	Metabolic Disease Inflammation/Immunology Cancer
Pamidronic acid (Standard) is the analytical standard of Pamidronic acid. This product is intended for research and analytical applications. Pamidronic acid, the second-generation nitrogen-containing bisphosphonate, is an inhibitor of bone loss. Pamidronic acid significantly inhibits subchondral bone loss in early osteoarthritis by upregulating the expression of OPG in cartilage and subchondral bone, and inhibiting the expression of RANKL and MMP-9 in both tissues, as well as TLR-4 in cartilage, thereby alleviating cartilage degeneration. Additionally, Pamidronic acid can inhibit the signaling of Wnt and β-catenin, and is applicable for research on osteoporosis and osteosarcoma .

E09241	Wnt β-catenin Nuclear Factor of activated T Cells (NFAT) MMP RANKL/RANK	Metabolic Disease
E09241 is an orally active osteoclastogenesis inhibitor. E09241 reduces the RANKL-induced expression of NFATc1 and MMP-9 by activating Wnt/β-catenin. E09241 increases the OPG/RANKL ratio by upregulating OPG expression, inhibits bone resorption, promotes bone formation and prevents ovariectomy-related bone loss. E09241 can be used in the research of osteoporosis .

Cat. No.	Product Name	Target	Research Area

TriDAP dihydrochloride 1 Publications Verification L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride	NOD-like Receptor (NLR) NF-κB MAP3K MEK ERK p38 MAPK Interleukin Related SARS-CoV	Infection Inflammation/Immunology
TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a K_d value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the *RANKL/OPG* ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection .

TriDAP L-Ala-γ-D-Glu-meso-diaminopimelic acid	NOD-like Receptor (NLR) NF-κB MAP3K MEK ERK p38 MAPK Interleukin Related SARS-CoV	Infection Inflammation/Immunology
TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a NOD1 agonist with a K_d value of 34.5 μM. TriDAP enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP decreases IκBα levels and increases p65 levels. TriDAP induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP increases the *RANKL/OPG* ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection .

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