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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

PubMedLangmuir : the ACS journal of surfaces and colloids2026-07-16

Development of a Citric Acid-Promoted Betaine Surfactant for an Integrated Fracturing-Oil Displacement Fluid System: Experimental and Nuclear Magnetic Resonance Studies.

Han Weiwei W, Chai Jiajie J, Xiang Wei W, Dong Sanbao S et al.

To address the growing demand for clean and efficient fracturing fluids suitable for low-permeability reservoirs, this study explored the impact of organic acids with varied molecular structures on the rheological behavior of erucic amide propyl betaine (EAPB) and developed an EAPB/citric acid (CA) clean fracturing fluid system. After 2 h of continuous shearing at 170 s-1 and 90 °C, the fluid viscosity retained 38 mPa·s. The system also showed excellent shear recovery ability even under a shear rate as high as 300 s-1. Although the EAPB/CA system initially showed limited salt resistance, the addition of ethylenediaminetetraacetic acid disodium salt (EDTA-2Na) and diethylenetriaminepenta (methylenephosphonic) acid (DTPMP) significantly enhanced its salt resistance. The fracturing fluid also demonstrated favorable sand-carrying performance (0.0003 mm·s-1) and anti-swelling efficiency (92%). With 30% kerosene, the viscosity dropped below 5 mPa·s within 30 min at 90 °C, and the surface tension decreased to 23.21 mN/m. At a gel-breaking fluid concentration of 0.3%, the interfacial tension reached 10-2 mN/m, and the contact angle shifted from 91° to 42°, indicating strong interfacial activity and wettability alteration that promoted crude oil stripping. To verify the dual fracturing-oil displacement function, static imbibition tests were performed using the gel-breaking fluid, achieving a spontaneous imbibition recovery of 45% at 60 °C. Nuclear magnetic resonance (NMR) results further confirmed that the gel-breaking fluid exhibited exceptional crude oil mobilization capability in small pores. These findings highlight the potential of the EAPB/CA system as an integrated fracturing and enhanced oil recovery fluid for low-permeability reservoirs.

PMID 42460616
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PubMedJournal of magnetic resonance imaging : JMRI2026-07-14

Effect of 37°C Pre-Warmed Versus Room Temperature Gadoxetic Acid Disodium Contrast Medium on Patient Comfort and Image Quality in Liver MRI: A Prospective, Double-Blind, Self-Controlled Before-and-After Study.

Feng Kanghua K, Xu Haifeng H, Li Minghao M, Su Luowei L et al.

Compromised patient comfort and suboptimal arterial phase (AP) image quality remain unresolved challenges in Gd-EOB-DTPA-enhanced liver MRI. To evaluate the effects of pre-warmed (37°C) Gd-EOB-DTPA contrast medium on patient comfort and image quality in liver MRI. Prospective, single-center, double-blind, self-controlled before-and-after study. One hundred and thirty-eight participants (113 males; mean age 56.33 ± 11.24 years) who underwent Gd-EOB-DTPA-enhanced liver MRI. 3.0-T; AP and Hepatobiliary phase (HBP) were both T1WI 3D spoiled gradient-echo dynamic sequences. The primary outcome of this self-controlled before-and-after study was to compare image quality of room temperature (25°C) and pre-warmed (37°C) contrast medium. A 4-point scale and an 11-Numeric Rating Scale were used to evaluate overall participant comfort, while a 4-point Likert scale was applied for image quality assessment. In vitro experiments were conducted to characterize the physicochemical properties of the contrast medium, and renal function parameters were measured to assess its nephrotoxicity. Paired t-test, Wilcoxon signed-rank test, and Stuart-Maxwell test; two-tailed p < 0.05 was significant. Significant differences were observed between 37°C and 25°C for participant comfort (comfortable or very comfortable rate: 97.1% vs. 82.6%), adverse sensations including dyspnea (incidence: 1.4% vs. 13.8%), and AP image quality (excellent rate: 50.0% vs. 0.7%). For the HBP, contrast-to-noise ratio (CNR) and liver-to-spleen contrast ratio (LSC) changes were not significant (p = 0.067, p = 0.079, respectively). In vitro, Gd-EOB-DTPA maintained stable chemical properties and its viscosity, shear stress, and torque decreased. Renal function showed no differences (urea p = 0.933, creatinine p = 0.249, endogenous clearance p = 0.206). Pre-warming Gd-EOB-DTPA to 37°C improves patient comfort, reduces adverse sensations, optimizes AP image quality, and maintains HBP image quality. 2. Stage 3.

PMID 42446484
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PubMedAngewandte Chemie (International ed. in English)2026-07-13

An Oligomeric Additive Bridges Inner and Outer Helmholtz Planes to Enable Reversible Zn Anodes via Spatial and Functional Decoupling.

Wang Yanjing Y, Zhou Le L, Zhang Tianyu T, Gao Wenzhuo W et al.

Precise molecular engineering of the electrode/electrolyte interface remains a key bottleneck for aqueous Zn-ion batteries (ZIBs). Here, we report an oxidative polymerization strategy to synthesize oligomeric chromotropic acid disodium salt (OCAD) as a multifunctional additive. The oligomeric architecture bridges the inner and outer Helmholtz planes (IHP and OHP), shifting regulation from IHP-localized adsorption to full IHP/OHP coverage. The expanded dimeric framework (1.51 vs. 0.65 nm) displaces water molecules and promotes Zn2+ desolvation at the OHP via steric hindrance and hydrophobic effects, while sulfonic and phenolic hydroxyl groups repel SO4 2- and buffer pH at the IHP through electrostatic repulsion and proton donation. This functional decoupling overcomes the consumption-driven failure of conventional small-molecule additives, suppressing side reactions and guiding uniform Zn deposition. Consequently, symmetric cells with OCAD-modified Zn anodes achieve exceptional cycling stability exceeding 4300 h at 1 mA cm-2/1 mAh cm-2 and operate at an 85.6% depth of discharge. A full battery paired with a Na2V6O16 cathode retains 81.6% capacity after 4700 cycles at 20 A g-1. The performance translates effectively to high‑mass‑loading cathodes and pouch cells, underscoring practical viability. This work establishes molecular oligomerization as a versatile paradigm for long‑range interface regulation in durable aqueous ZIBs.

PMID 42441730
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PubMedGlia2026-07-09

Microglial P2ry12 in the Basolateral Amygdala Underlies Neuropathic Pain-Induced Anxiety.

Yang Xiaohui X, Chen Li L, Shi Qiuxiao Q, Liu Hanmin H et al.

Anxiety is a common clinical comorbidity of neuropathic pain. The basolateral amygdala (BLA) is critically involved in both pain and anxiety processing. Microglia have emerged as key regulators of neuronal plasticity, and disruption of homeostatic neuron-microglia crosstalk can precipitate neuropsychiatric disorders. Although microglia are abundant in the BLA, their specific role in modulating neuronal plasticity underlying pain-induced anxiety remains poorly understood. Here, we demonstrate that spared nerve injury (SNI) induces anxiety-like behaviors in mice, accompanied by neuronal hyperexcitability and increased spine density in the BLA. These changes correlated with increased density of hyper-ramified microglia, along with upregulated P2ry12 expression and enhanced microglial BDNF production. Importantly, microglial P2ry12 knockdown significantly attenuated both process hyper-ramification and BDNF overexpression in the BLA. Furthermore, either microglial depletion with clodronate or microglial P2ry12 knockdown in the BLA reversed neuronal hyperexcitability and spine overgrowth, and alleviated pain and anxiety-like behaviors in SNI mice. Meanwhile, clodronate mildly suppressed neuronal excitability and dendritic spine density in the BLA of control mice, whereas P2ry12 knockdown had no detectable impact on these neuronal measures. Together, these findings support a role for microglia in maintaining physiological neuronal excitability and spine density. Highly-ramified microglia and their increased P2ry12 expression underlie the enhanced neuronal excitability and spine density in the BLA, thereby promoting comorbidity of pain and anxiety.

PMID 42423185
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PubMedBiochemical pharmacology2026-07-08

Revisiting pharmacological actions of disodium cromoglycate in light of GPR35: New therapeutic contexts for classical drugs.

Tanaka Satoshi S

Mast cell stabilizers such as disodium cromoglycate have been used for decades as prophylactic anti-allergic agents, yet their molecular targets remained unknown, and their intracellular mechanisms were long debated. Identification of GPR35 as a receptor engaged by multiple mast cell stabilizers provided a new framework to reinterpret classical pharmacology. Here, historical and recent evidence linking mast cell stabilizers to GPR35 is integrated and pharmacological characteristics of GPR35 are described in the context of species difference and intracellular signaling. GPR35 is expressed in epithelial, myeloid, and sensory neuronal compartments, raising the possibility that some "mast cell stabilizer" phenotypes reflect actions outside mast cells. This perspective becomes particularly relevant in inflammatory bowel disease, where genetic studies support a protective role for GPR35 in mucosal homeostasis, potentially through epithelial barrier integrity and macrophage function. Emerging data also implicate GPR35 in neurogenic inflammation/itch pathways and vascular remodeling, further broadening therapeutic considerations. Accumulating evidence suggests that GPR35 exhibits physiologically relevant constitutive activity, implying that the GPR35-mediated actions may depend not only on ligand engagement but also on expression levels and cellular states. Implications for drug repositioning of mast cell stabilizers and future GPR35-targeted therapeutics are also discussed.

PMID 42413736
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PubMedInternational immunopharmacology2026-07-08

Dioscin suppresses colitis-associated colorectal tumorigenesis by inhibiting PPARγ-mediated fatty acid oxidation in TAMs.

Xun Jing J, Jiang Xiaolin X, Zhang Jinlu J, Liu Bin B et al.

Chronic inflammation plays a key role in colorectal carcinogenesis, where tumor-associated macrophages (TAMs) critically promote tumor progression. Metabolic reprogramming of TAMs, particularly through the modulation of fatty acid oxidation (FAO), represents a promising therapeutic strategy; however, effective agents remain to be identified. Although the natural compound dioscin exhibits anti-tumor properties, its ability to regulate TAM plasticity and metabolism in colitis-associated colorectal cancer (CAC) remains unclear. A mouse model of CAC was established using azoxymethane/dextran sulfate sodium (AOM/DSS). Mice were treated with dioscin, and tumor development was monitored. Bone marrow-derived macrophages were polarized into TAMs, and the effects of dioscin on polarization and metabolism were evaluated by flow cytometry, immunohistochemistry, Seahorse analysis, and biochemical assays. Systemic macrophage depletion assay via clodronate liposomes validated the necessity of TAMs. Molecular docking, CETSA, and DARTS assays identified the direct target of dioscin. Pharmacological or genetic modulation of PPARγ confirmed mechanistic necessity. Dioscin significantly suppressed colorectal tumorigenesis in vivo. This efficacy was abolished upon macrophage depletion, confirming TAMs dependency. Dioscin modulated the TAMs polarization by primarily suppressing the M2 phenotype, leading to an increase in the M1/M2 ratio. Mechanistically, dioscin directly bound to PPARγ, suppressing its expression and downstream CPT1A-mediated FAO. Seahorse analysis revealed impaired spare respiratory capacity. Notably, while FAO inhibition coincided with increased lactate production, glycolytic flux and gene expression remained unaltered. Both pharmacological activation and genetic ablation of PPARγ abrogated dioscin-induced FAO inhibition and TAMs polarization. Our study demonstrates that dioscin inhibits colorectal carcinogenesis by directly targeting PPARγ in TAMs, leading to the suppression of FAO and a consequent reduction in M2 polarization. These findings establish dioscin as a promising candidate for future therapeutic strategies targeting the immunosuppressive tumor microenvironment.

PMID 42413310
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