Neridronate sodium

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Neridronate sodium is a bisphosphonate. Bisphosphonates initiate the Apoptotic process. Neridronate sodium reduces the levels of bone resorption, bone turnover markers, the degree of back pain, and the risk of fractures. Neridronate sodium inhibits capillary tube formation. Neridronate sodium itself has weak anticancer activity, but liposomal encapsulation enhances this activity. Neridronate sodium can be used in research related to demineralizing metabolic bone diseases, thalassemia-associated osteoporosis, chronic inflammatory diseases, cancer, and osteogenesis imperfecta.

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Neridronate sodium Chemical Structure

CAS No. : 80729-79-9

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Other In-stock Forms of Neridronate sodium:

Neridronate

Other Forms of Neridronate sodium:

Neridronate In-stock

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Biological Activity
Purity & Documentation
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Description

In Vitro

Neridronate sodium alters the biosynthetic activity of osteoblasts in vitro, which may affect bone turnover rate^[2].
Neridronate (1-50 μM; 24 h) sodium inhibits the proliferation of human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner, with the inhibitory effect peaking at 30 μM and reaching a plateau at 50 μM^[3].
Neridronate (30 μM; 18 h) sodium disrupts the formation of capillary-like tubes by umbilical vein endothelial cells (HUVECs) cultured on Matrigel, which is induced by fibroblast growth factor-2 (FGF-2)^[3].
Liposomal neridronate (0.27-17.56 μM; 24-72 h) sodium potently inhibits the viability of MDA-MB-231, U87-MG and Caco2 cancer cells, with an EC₅₀ of 1.7 μM after 72 h of incubation in MDA-MB-231 cells; in contrast, free neridronate (16 μM-1 mM; 72 h) exerts weak inhibitory effects on these cell lines^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[3]

Cell Line:	human umbilical vein endothelial cells (HUVECs)
Concentration:	1 μM, 3 μM, 10 μM, 30 μM, 50 μM
Incubation Time:	24 h
Result:	Reduced HUVEC growth in a dose-dependent fashion, with the maximum inhibitory effect observed at 30 μM; the effect plateaued at 50 μM. Significantly inhibited HUVEC proliferation at 10 μM, 30 μM, and 50 μM relative to lower concentrations.

Cell Viability Assay^[4]

Cell Line:	MDA-MB-231 human breast carcinoma cells, U87-MG human brain carcinoma cells, Caco2 human colon carcinoma cells
Concentration:	16 μM-1 mM (free neridronate); 0.27 μM-17.56 μM (liposomal neridronate)
Incubation Time:	72 h (free neridronate); 24 h, 48 h, 72 h (liposomal neridronate)
Result:	Achieved maximum growth inhibition of 46% in MDA-MB-231 cells (EC₅₀ = 95 μM), 52% in U87-MG cells (EC₅₀ = 14 μM), and 37% in Caco2 cells (EC₅₀ = 130 μM) after 72 h of free neridronate treatment. Achieved maximum growth inhibition of 100% in MDA-MB-231 cells (EC₅₀ = 1.7 μM), 70% in U87-MG cells (EC₅₀ = 1 μM), and 62% in Caco2 cells (EC₅₀ = 4 μM) after 72 h of liposomal neridronate treatment. Achieved 100% growth inhibition in MDA-MB-231 cells with an EC₅₀ of 2.4 μM after 48 h of liposomal neridronate treatment.

In Vivo

Neridronate (50 μM/embryo; administered locally via gelatin sponge implantation; single dose) sodium significantly reduces FGF-2-induced angiogenesis in the chick embryo CAM assay, decreasing the average number of blood vessels from 30 to 15^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	White Leghorn (fertilized embryos)^[3]
Dosage:	50 μM/embryo
Administration:	local administration via gelatin sponge implant; single dose
Result:	Reduced mean number of vessels entering the sponge to 15, compared to the FGF-2-only control mean of 30.

Molecular Weight

299.13

Formula

C₆H₁₆NNaO₇P₂

CAS No.

80729-79-9

SMILES

NCCCCCC(P(O)(O[Na])=O)(O)P(O)(O)=O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Nicolin V, et al. Effects of neridronic acid on osteoclasts derived by physiological dual-cell cultures. Acta Histochem. 2007;109(5):397-402. [Content Brief]

[2]. Forni GL, et al. Neridronate improves bone mineral density and reduces back pain in β-thalassaemia patients with osteoporosis: results from a phase 2, randomized, parallel-arm, open-label study. Br J Haematol. 2012 Jul;158(2):274-282. [Content Brief]

[3]. Ribatti D, et al. Neridronate inhibits angiogenesis in vitro and in vivo. Clin Rheumatol. 2007 Jul;26(7):1094-8. [Content Brief]

[4]. Chebbi I, et al. In vitro assessment of liposomal neridronate on MDA-MB-231 human breast cancer cells. Int J Pharm. 2010 Jan 4;383(1-2):116-22. [Content Brief]

[5]. Gatti D, et al. Intravenous neridronate in children with osteogenesis imperfecta: a randomized controlled study. J Bone Miner Res. 2005 May;20(5):758-63. [Content Brief]