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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

PubMedJournal of medicinal chemistry2026-11-12

A Novel Small-Molecule Antagonist of the NOD1 Signaling Pathway as a Therapeutic Strategy for Acute Pancreatitis.

Liu Xinhua X, Wang Dan D, Wang Yuting Y, Zhang Nan N et al.

Acute pancreatitis (AP) is a sterile inflammatory disease characterized by aberrant zymogen activation, tissue autodigestion, and cross-amplifying inflammatory cascades that complicate targeted therapies. Our single-cell transcriptomics analysis revealed early NOD1 pathway activation in pancreatic acinar and ductal cells in cerulein-induced AP mice, suggesting potential involvement across these cell types. Here, through a scaffold-hopping strategy, we obtained novel-scaffold NOD1 antagonists. Further optimization yielded 32q and its highly water-soluble disodium salt, 32q-2Na. They exhibited low-nanomolar potency against NOD1 with high selectivity. 32q-2Na pharmacologically inhibited NOD1 signaling, significantly reducing serum levels of amylase (AMY), lipase (LIP), MCP-1, and IL-6, and markedly attenuating pancreatic inflammatory responses in cerulein- and FAEE-induced murine models of AP. In conclusion, these findings establish NOD1 as a highly tractable upstream regulatory node for AP intervention.

PMID 43018575
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PubMedEmerging microbes & infections2026-11-12

Immune control of lethal Nipah virus infection: the critical role of host macrophages.

Ronco Ilona I, Dhondt Kévin K, Iampietro Mathieu M, Moroso Marie M et al.

AbstractNipah virus (NiV) is highly pathogenic zoonotic paramyxovirus of Henipavirus genus that causes recurrent human outbreaks in South-East Asia, with a lethality of 40-75%. Immunopathogenesis associated to this emerging virus is still poorly understood and the role of different components of the immune response in the control of infection remains unknown. In contrast to many other mammalian species, wild type mice are resistant to NiV infection, due to an efficient type-I interferon response. We have analysed the role of various immune cell populations in the control of NiV infection and demonstrated the critical role of T lymphocytes but neither B lymphocytes nor NK cells were primordial. In addition, the depletion of phagocytes in mice by injection of clodronate liposomes resulted in dramatical increase of their susceptibility to NiV infection. Moreover, using CD169-DTR transgenic mice we show here that the specific depletion of CD169+ macrophages results in an increased susceptibility of mice to NiV challenge, highlighting the important role of this cell population. Finally, in NiV-infected African green monkeys, which closely resemble severe human Nipah disease, the production of virus-induced type-I and -II interferons was followed with an important increase of CD169+ cells in the blood and lungs, with some of them being NiV-infected. As CD169+ macrophages have been described to play an important role at the crossroads between innate and adaptive immunity in various infections, these results reveal their potentially determining role during NiV infection as well, which may help to better understand this highly lethal infectious disease.

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PubMedAbdominal radiology (New York)2026-11-11

T1 mapping-based heterogeneity analysis of Gd-EOB-DTPA-enhanced MRI in cirrhotic nodules: biological basis, emerging evidence, and future perspectives.

Zhou Chenli C, Luo Yindeng Y

Liver cirrhosis is a major risk factor for hepatocellular carcinoma (HCC), and accurate risk stratification of cirrhotic nodules remains a clinical challenge. During hepatocarcinogenesis, regenerative and dysplastic nodules undergo heterogeneous alterations in hepatocyte function, transporter expression, vascular architecture, and tissue composition. However, conventional magnetic resonance imaging (MRI) assessment of intranodular signal heterogeneity largely relies on subjective visual interpretation and lacks standardized and reproducible quantitative biomarkers. Gadoxetic acid disodium (Gd-EOB-DTPA)-enhanced MRI provides functional information during the hepatobiliary phase by reflecting hepatocyte-specific uptake mediated by organic anion transporting polypeptides. Impaired transporter expression during malignant transformation is associated with reduced contrast uptake and may contribute to spatially heterogeneous contrast distribution. Quantitative T1 mapping enables voxel-wise measurement of absolute T1 relaxation times, thereby providing an objective and quantitative approach to tissue characterization. However, most existing studies have primarily focused on mean T1 values or global reduction rates, while intranodular spatial heterogeneity remains insufficiently explored. MRI-based heterogeneity analysis may complement conventional mean-value analysis by capturing regional variations within lesions. However, direct evidence on T1 mapping-derived heterogeneity in cirrhotic nodules remains limited, and its incremental value over mean T1 values for reflecting hepatocellular function or early malignant transformation has not been established. Quantitative heterogeneity descriptors, including standard deviation, coefficient of variation, histogram-based parameters, and texture features, can objectively characterize the magnitude and distribution of spatial T1 variation and provide a quantitative framework for assessing intralesional heterogeneity. This review summarizes the biological rationale, technical principles, and emerging evidence regarding Gd-EOB-DTPA-enhanced T1 mapping for the assessment of intranodular heterogeneity. It further discusses its potential role in malignant transformation risk stratification of cirrhotic nodules, current limitations, and future directions for clinical translation.

PMID 43012971
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PubMedCancer research2026-11-09

Tumor Cells Hijack Coagulation Signaling to Enable Immune Escape and Metastatic Dissemination.

Wang Shuang S, Lin Jiliang J, Zhao Zhou-Kai ZK, Zhang Baishen B et al.

Lymph node metastasis (LNM) represents a pivotal event in cancer progression and a major determinant of response to immune checkpoint blockade (ICB). Elucidation of the molecular mechanisms linking metastatic dissemination to immune suppression could identify potential therapeutic targets to improve ICB efficacy. Here, we identified the coagulation initiator tissue factor (F3) as a central regulator bridging tumor metastasis and immune evasion in gastric cancer (GC). F3 was significantly upregulated in LNM-positive tumors and correlated with impaired ICB responsiveness and poor clinical outcome. Mechanistically, the intracellular domain of F3 directly bound eEF1A1 to promote STAT3 phosphorylation and induce CCL20 expression, which selectively recruited CCR6+ regulatory T cells (Tregs) to establish an immunosuppressive microenvironment. Disruption of this F3-eEF1A1-STAT3-CCL20 axis with the clinically approved compound olsalazine disodium served as a compelling preclinical proof-of-concept to potently suppress tumor growth, abrogate Treg infiltration, and restore ICB sensitivity, all without perturbing basal coagulation. These findings redefine F3 from a canonical coagulation initiator to a tumor-intrinsic immunomodulator and reveal a druggable vulnerability that uncouples its oncogenic signaling from hemostasis.

PMID 43002440
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PubMedActa crystallographica. Section E, Crystallographic communications2026-11-08

Syntheses and structures of trans-di-aqua-bis(propane-1,3-di-amine-κ2 N,N')nickel(II) salts of two isomeric naphthalene-disulfonates.

Squattrito Philip J PJ, Gianopoulos Christopher G CG

Aqueous reactions of nickel(II) nitrate, propane-1,3-di-amine, and either naphthalene-1,5-di-sulfonic acid or disodium naphthalene-2,6-di-sulfonate produced crystals of trans-di-aqua-bis-(propane-1,3-di-amine-κ2 N,N')nickel(II) naphthalene-1,5-di-sulfonate, (I), and trans-di-aqua-bis-(propane-1,3-di-amine-κ2 N,N')nickel(II) naphthalene-2,6-di-sulfonate, (II), both [Ni(C3H10N2)2(H2O)2](C10H6O6S2), in high yields. (I) crystallizes in the monoclinic space group P21/c while (II) crystallizes in the triclinic space group P1. In both structures, the cation and anion rest on centers of inversion. The nickel cations display trans octa-hedral coordination of two water mol-ecules and two bidentate propane-1,3-di-amine mol-ecules with Ni-O/N bond distances in the ranges 2.0960 (9)-2.1205 (7) Å (I) and 2.1110 (7)-2.1181 (9) Å (II). The packing in both structures features alternating layers of complex cations and naphthalene-disulfonate anions held together by O-H⋯O and N-H⋯O hydrogen bonds between the water and amine groups of the ligands and the sulfonate groups of the anions. These are the first metal salts of naphthalene-1,5-di-sulfonate and naphthalene-2,6-di-sulfonate that contain propane-1,3-di-amine. The packing in (I) and (II) is compared to each other and to those found in other nickel salts of the anions.

PMID 42997408
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PubMedClinical case reports2026-11-06

When the Antibiogram Offers Nothing Else: Ceftriaxone-Sulbactam-Disodium EDTA With Intravenous Colistin in Two Neonates With Metallo-β-Lactamase-Producing Acinetobacter baumannii Meningitis.

Puri Naini N, Shubham Shantanu S, Ahmed Syed Moiz SM, Joshi Richa R et al.

Two neonates with metallo-β-lactamase-producing Acinetobacter baumannii meningitis, resistant to every tested alternative, received ceftriaxone-sulbactam-disodium EDTA plus intravenous colistin, which, to our knowledge, represents the first reported neonatal use of this combinations. Cultures were sterilized by day 7; both survived with normal assessments at 3-months. Concomitant colistin precludes attributing the response to either agent.

PMID 42991875
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