Drug Database
CL

clodronate disodium (Bonefos / Clastoban)

✓ Approved

Takeda · SLC17A9 · Small Molecule

What is clodronate disodium?

clodronate disodium is a small molecule developed by Takeda. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesBonefos, Clastoban
CompanyTakeda
Drug ClassSmall Molecule
Molecular TargetSLC17A9
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Takeda

Mechanism of Action

Molecular Targets

clodronate disodium acts on 1 molecular target:

SLC17A9solute carrier family 17 member 9 (POROK8, VNUT)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

clodronate disodium is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Endocrine disordersHypercalcaemia of malignancy✓ Approved
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

Related Research Articles

PubMedPolymers2026-09-15

Multifunctional Flame-Retardant, Hydrophobic, and Antifungal Boron-Silane Synergistic Coating for Archival Packaging Materials.

Wang Juanli J, Xie Qingyang Q, Tian Ye Y, Tian Jiayao J

Kraft paper, as a typical archival packaging material, is prone to microbial erosion, flammability, and moisture-induced degradation during long-term preservation. In this work, multifunctional archival packaging paper with integrated flame retardancy, antifungal activity, and hydrophobicity was successfully fabricated via the modification of boron-based flame retardants (borax, BX, and disodium octaborate tetrahydrate, DOT) and silane hydrophobic agent (octadecyltrimethoxysilane, ODTMS). The structure and performance of the modified kraft paper were systematically characterized by the limiting oxygen index (LOI), the vertical burning test, cone calorimetry (CCT), thermogravimetric analysis (TGA), X-ray photoelectron spectroscopy (XPS), contact angle measurement, and the antifungal test. The optimized modified sample exhibited superior comprehensive properties. The LOI value increased from 20.6% for the original kraft paper to 37.5%. TGA revealed that the char residue of the optimized modified sample at 750 °C reached up to 55.35%, much higher than that of the original kraft paper, accompanied by marked decreases in the heat release rate, total heat release, and smoke production. Meanwhile, ODTMS endowed the modified sample with hydrophobic properties, with a water contact angle of approximately 130°. Antifungal tests demonstrated that the modified kraft paper displayed obvious inhibitory effects against eight fungal species, including Penicillium citrinum and Aspergillus flavus. Overall, the modification strategy proposed in this study is simple, eco-friendly, and low-cost, achieving multifunctional protection of archival packaging materials. This work is expected to provide novel materials and technical support for the long-term safe preservation of paper cultural relics and archives.

PMID 42737177
Read full article →
PubMedRadiology case reports2026-09-14

Hepatic mesenchymal hamartoma showing hepatobiliary-phase signal increase on gadoxetate disodium-enhanced magnetic resonance imaging: A case report.

Sugie Tsubasa T, Tsuchiya Nanae N, Kinjo Shota S, Kuda Masaaki M et al.

We report a case of a 9-month-old girl with mesenchymal hamartoma that was evaluated using gadoxetate disodium-enhanced magnetic resonance imaging. Imaging revealed a large hepatic mass with mixed cystic and solid components, with a slight signal increase in the solid component during the hepatobiliary phase. Histopathology confirmed mesenchymal hamartoma, with normal hepatic parenchyma reticularly interspersed within the mass. Immunohistochemical staining for organic anion transporting polypeptide 1B3 showed cytoplasmic immunoreactivity without membranous staining in hepatocyte-like cells. Mesenchymal hamartoma is a rare benign liver tumor in children, accounting for approximately 8% of all pediatric hepatic tumors. This case suggests that mesenchymal hamartoma may show a slight hepatobiliary-phase signal increase, potentially reflecting delayed contrast retention within the interstitium of the solid component.

PMID 42733421
Read full article →
PubMedInternational immunopharmacology2026-09-13

Batf2 knockdown ameliorates early-stage hyperoxia-induced BPD-like lung injury and is associated with suppression of GBP5/NF-κB signaling.

Duan Shanshan S, Gou Zhixian Z, Xu Honghao H, Wang Hui H et al.

Bronchopulmonary dysplasia (BPD) is characterized by persistent inflammation and impaired alveolar development. Macrophage inflammatory dysregulation contributes to BPD progression, but its upstream regulators remain incompletely understood. This study investigated the role of Batf2 in hyperoxia-induced lung injury and its potential association with GBP5/NF-κB signaling. Batf2 was initially screened using the peripheral blood transcriptomic dataset GSE32472. An early-stage hyperoxia-induced BPD-like lung injury model in neonatal mice and an LPS-stimulated RAW264.7 inflammatory macrophage model were used for in vivo and in vitro validation, respectively. Macrophages were depleted using clodronate liposomes, and Batf2 was silenced using adenoviral shRNA in vivo and siRNA in vitro. Alveolar development and macrophage polarization-related changes were evaluated by histological staining, radial alveolar count, western blotting, RT-qPCR, immunofluorescence staining, and flow cytometry. RNA sequencing, GBP5 knockdown, and GBP5 overexpression rescue experiments were performed to investigate downstream mechanisms. Batf2 expression was increased in BPD-related peripheral blood transcriptomic data, hyperoxia-exposed neonatal lungs, and LPS-stimulated RAW264.7 macrophages. Hyperoxia induced alveolar simplification and a pro-inflammatory macrophage-associated phenotype, whereas macrophage depletion attenuated lung injury. Batf2 knockdown improved alveolar development, reduced M1-associated and pro-inflammatory markers, and restored M2-associated markers. RNA sequencing identified Gbp5 as a Batf2-associated candidate gene. GBP5 overexpression partially reversed the changes in iNOS and Arg1 induced by Batf2 silencing, whereas GBP5 knockdown reduced inflammatory mediators and suppressed NF-κB p65 phosphorylation and nuclear translocation. In hyperoxia-exposed lung tissues, Batf2 knockdown was also associated with reduced GBP5 expression and p65 phosphorylation. Batf2 knockdown alleviates early BPD-like alveolar injury and macrophage-associated inflammatory responses in hyperoxia-exposed neonatal mice. GBP5/NF-κB signaling may partially contribute to Batf2-associated inflammatory regulation, although the cellular and molecular causality of this pathway requires further validation.

PMID 42732671
Read full article →
PubMedNeurochemical research2026-09-11

Pathophysiological Role of Perivascular Macrophages in Blood-Brain Barrier Dysfunction Induced by Cerebral Hypoperfusion in Mice.

Matsumura Sayaka S, Moriyama Yoshiyuki Y, Ochiai Ayumi A, Iwatani Yui Y et al.

This study investigated the role of perivascular macrophages (PVMs), localized alongside the brain vasculature, in blood-brain barrier (BBB) dysfunction induced by reduced cerebral blood flow (CBF). Using a mouse model of bilateral carotid artery stenosis (BCAS) to examine cerebral hypoperfusion, the effects of pharmacological depletion of PVM-enriched macrophage populations were examined using clodronate liposomes. The results demonstrated that while cerebral hypoperfusion significantly increased BBB permeability, depletion of PVM-enriched macrophage populations attenuated this leakage. Mechanistic analyses suggested that PVM-associated responses may be linked to reduced pericyte marker expression, astrocyte activation, and increased MMP-2/9 expression. Furthermore, depletion of PVM-enriched macrophage populations inhibited the upregulation of matrix metalloproteinase-2 (MMP-2) and MMP-9. These findings suggest that PVM-enriched macrophage populations are involved in early BBB dysfunction following cerebral hypoperfusion, possibly through changes in pericyte-associated vascular integrity, astrocyte activation, and MMP-2/9-related tight junction remodeling. These results provide insight into vascular inflammatory mechanisms that may contribute to hypoperfusion-associated BBB dysfunction and later small vessel pathology.

PMID 42726381
Read full article →
PubMedJournal of hazardous materials2026-09-09

HIF-1α-associated macrophage metabolic reprogramming mediates intestinal injury induced by acrylamide and 5-hydroxymethylfurfural co-exposure.

Lu Jiawen J, Shen Yangchun Y, Zhou Xingtao X, Wang Yuting Y et al.

Acrylamide (AA) and 5-hydroxymethylfurfural (HMF) are processing-derived contaminants that frequently co-occur in environmental and dietary exposure, yet the health effects of their co-exposure remain poorly understood. Here, we show that co-exposure to AA and HMF induces duodenal injury in mice, whereas neither toxin alone causes significant damage. Macrophage depletion using clodronate liposomes significantly attenuates this pathology, identifying macrophages as important mediators of the intestinal injury. Co-exposure promotes macrophage polarization toward a pro-inflammatory phenotype. Notably, direct exposure of intestinal epithelial cells to AA and HMF produces limited cytotoxicity. In contrast, conditioned medium from AA+HMF-treated macrophages compromises epithelial viability and barrier integrity in both intestinal epithelial cells and mouse intestinal organoids. These findings indicate that macrophage-mediated inflammatory responses, rather than direct epithelial toxicity, contribute substantially to AA+HMF-induced intestinal injury. Mechanistically, AA and HMF co-exposure triggers mitochondrial dysfunction and elevated mitochondrial reactive oxygen species (mtROS) production in macrophages, accompanied by enhanced glycolysis and hypoxia-inducible factor-1α (HIF-1α) activation. Pharmacological inhibition or genetic silencing of HIF-1α attenuates metabolic and inflammatory responses, while scavenging mtROS or iNOS inhibition reduces macrophage activation. Collectively, these findings reveal an immune-mediated mechanism underlying AA and HMF co-exposure-induced intestinal injury and highlight macrophage responses as a determinant of contaminant mixture toxicity.

PMID 42715669
Read full article →
PubMedJournal of fish biology2026-09-09

Taste preferences of tiger puffer (Takifugu rubripes) to common amino acids and feed attractants.

Ye Zhengwei Z, Liu Jiahao J, Zhang Yanjiao Y, Li Haoxuan H et al.

The taste preferences of fish which directly influence the feeding action are diversified among species. The present study evaluated the taste preference of tiger puffer (Takifugu rubripes) to a number of compounds including an achiral amino acid (glycine), 16 L-amino acids, 15 D-amino acids and seven commonly used feed attractants. A total of 18 intact and healthy tiger puffers (initial body weight 43.33 ± 3.91 g) were randomly separated in nine 100-L tanks (two fish in each tank as one statistical unit). The test compounds were added in aqueous agar solution to make test pellets. Five parameters indicating the response of fish to pellets, namely, pellet grasp number (GN), ingestion ratio (IR, %), touch span (TS), rejection number (RN) and palatability index (PI), were used for the evaluation of feed palatability, based on which the test compounds were finally identified as attractive, indifferent or repulsive. The Spearman correlation analysis revealed that there was a significant correlation among GN, IR, RN and TS (p < 0.05). The L/D-alanine, L/D-proline, L-serine, L-histidine, glycine and inosine-5'-monophosphate disodium salt octahydrate, whose IR (over 90%) is significantly higher than that of the control, were identified as attractive (p < 0.05). This investigation provided basic information about the taste preferences of tiger puffer to potential feed attractants.

PMID 42712100
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about clodronate disodium