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clodronate disodium (Abioklad / Mebonat / Ostac)

✓ Approved

Abiogen Pharma S.p.A. · SLC17A9 · Small Molecule

What is clodronate disodium?

clodronate disodium is a small molecule developed by Abiogen Pharma S.p.A.. It is approved for therapeutic indications via injectable (others) or intraarterial injection or intramuscular (im) injection.

Drug Profile

Brand NamesAbioklad, Mebonat, Ostac
CompanyAbiogen Pharma S.p.A.
Drug ClassSmall Molecule
Molecular TargetSLC17A9
RouteInjectable (Others), Intraarterial Injection, Intramuscular (IM) Injection
StatusApproved
Sources: ClinicalTrials.gov, Abiogen Pharma S.p.A.

Mechanism of Action

Molecular Targets

clodronate disodium acts on 1 molecular target:

SLC17A9solute carrier family 17 member 9 (POROK8, VNUT)
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Therapeutic Indications

clodronate disodium is developed for 6 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Endocrine disordersHypercalcaemia of malignancy✓ Approved
Musculoskeletal and connective tissue disordersMusculoskeletal pain✓ Approved
Musculoskeletal and connective tissue disordersOsteoarthritis✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Cancer pain✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Breast cancerPhase III

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Related Research Articles

PubMedInternational journal of molecular sciences2026-10-16

Effect of Clodronate on the Pathogenesis in a Mouse Model of Lysosomal Acid Lipase Deficiency.

Mashima Ryuichi R, Takada Shuji S, Murayama Kei K, Hamazaki Takashi T

Lysosomal acid lipase deficiency (LAL-D, OMIM #309900), caused by mutations of the LIPA gene, is involved in two continuum disease phenotypes: Wolman disease in infants and cholesteryl ester storage disease in adults. Their major phenotypes include steatosis, hepatomegaly, splenomegaly, and elevated liver enzymes. Enzyme replacement therapy has been used for the treatment of LAL-D. In this study, we examined the therapeutic effect of liposomal clodronate in an LAL-D mouse model. When liposomal clodronate was administered intraperitoneally by a single administration at 200 mg/kg to adult mice, organ cholesterol and triglyceride levels partially decreased. Furthermore, a significant correction of the relative organ weight of the liver and spleen as well as a reduction in splenic lipids were observed when liposomal clodronate was administered at 50 mg/kg to young mice intraperitoneally by multiple administrations. These results demonstrate that liposomal clodronate might have a therapeutic effect on the LAL-D mouse model.

PMID 42883938
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PubMedRSC advances2026-10-15

Synergistic collaboration between an emulsifier, surfactant and penetrant for rapid low-shear emulsification to enhance heavy-oil recovery.

Ruan Jingxin J, Yang Huohai H, Chen Xin X, Xu Chengjun C et al.

Developing a viscosity reducer that can rapidly emulsify heavy oil and reduce its viscosity under low shear conditions is crucial for improving the oil recovery efficiency but remain a challenge unsolved. In this paper, a high-performance emulsifier (sodium isomeric tridecanol polyoxyethylene ether phosphate, E-1311P), a surfactant (disodium 4-dodecyl-2,4'-oxydibenzenesulfonate, DPEDS-12) and penetrant (methyl 3-nonenoate, M3N) were introduced and evaluated for enhance heavy-oil recovery. The emulsification and viscosity reduction performance of the emulsifier-surfactant-penetrant formulation was systematically evaluated through measurements of viscosity reduction, emulsification time, droplet size, oil-water interfacial tension, contact angle, and core-flooding performance. The addition of DPEDS-12 and M3N markedly improved the overall performance of E-1311P, with the optimal formulation comprising 0.30 wt% E-1311P, 0.10 wt% DPEDS-12, and 0.05 wt% M3N. At a shear rate of 7.34 s-1, this formulation achieved a viscosity reduction of 90-95% within 2-8 min, lowered the oil-water interfacial tension to 2.0 mN m-1, and reduced the contact angle to 33°. Core-flooding experiments yielded a cumulative oil recovery of 36.7%. Molecular dynamics simulations attributed the rapid low-shear emulsification to enhanced hydrophilicity, reduced steric hindrance, and accelerated molecular diffusion and penetration into heavy oil. These results demonstrate the multiscale synergy among the emulsifier, surfactant, and penetrant and highlight the great potential for enhancing heavy-oil recovery.

PMID 42877670
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PubMedTrials2026-10-14

Evaluating sedation efficacy and perioperative safety of fospropofol disodium versus propofol in elderly patients undergoing elective TURP: study protocol for a randomized controlled trial.

Sui Hongyuan H, Wu Tong T, Gao Lijuan L, He Qingying Q et al.

Fospropofol disodium is the first novel water-soluble propofol prodrug in China. After administration, it is mainly converted to propofol by alkaline phosphatase on the surface of endothelial cells to exert its pharmacological effects. Compared with propofol, fospropofol disodium has the characteristics of longer duration of action, lower incidence of injection pain and adverse events related to the respiratory and circulatory systems, and no adverse reactions related to lipid metabolism. At present, there are few reports on the safety and efficacy of fospropofol disodium in the induction and maintenance of general anesthesia. Therefore, this study aims to evaluate the safety and efficacy of fospropofol disodium in routine anesthesia for elective surgery in the elderly, so as to provide new medication guidance for its application in the induction and maintenance stages of general anesthesia in the elderly population. Seventy elderly patients aged 65-85 years with American Society of Anesthesiologists (ASA) physical status II or III, scheduled for elective transurethral resection of the prostate under general anesthesia, will be enrolled. Patients will be randomly divided into the propofol group (group E) and the fospropofol disodium group (group F) using a random number table, with 35 cases in each group. Anesthesia induction: sufentanil 0.2-0.4 µg/kg and cisatracurium besilate 0.15 mg/kg will be administered intravenously. Group E will receive an intravenous bolus of propofol 1-1.5 mg/kg, while group F will receive an intravenous bolus of fospropofol disodium 10-15 mg/kg, both infused within 60 s. Tracheal intubation will be performed when the patient's Modified Observer's Assessment of Alertness/Sedation (MOAA/S) score decreases to 1 with BIS < 60 sustained for ≥3 min, followed by routine mechanical ventilation. For anesthesia maintenance, group E will receive continuous intravenous infusion of propofol 4-12 mg/(kg·h) and remifentanil 0.2-0.4 µg/(kg·min) via a syringe pump; group F will receive continuous intravenous infusion of fospropofol disodium 10-20 mg/(kg·h) and remifentanil 0.2-0.4 µg/(kg·min) via a syringe pump. During the operation, the infusion rates of maintenance anesthetics will be adjusted according to hemodynamic status to maintain blood pressure and heart rate fluctuations within 20% of the baseline values, and the Bispectral Index (BIS) value will be maintained between 40 and 60. After the operation, patients will be transferred to the post-anesthesia care unit (PACU). Primary outcomes of this study: success rate of sedation and time to onset of sedation. (1) perioperative indicators, (2) hemodynamic indices at each time point, (3) adverse reactions. Elderly patients undergoing transurethral resection of the prostate (TURP) are often complicated with multiple comorbidities, leading to a relatively high anesthetic risk. This trial takes the success rate of sedation and time to onset of sedation as the primary endpoints, to compare the application differences between fospropofol disodium and propofol. The aim of this study is to evaluate the safety and efficacy of fospropofol disodium in routine anesthesia for elective surgeries in the elderly population. The study was registered at the Chinese Clinical Trials Registry (ChiCTR2500115343) on December 24, 2025 ( http://www.chictr.org.cn/showproj.html?proj=294899 ).

PMID 42870298
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PubMedBJR case reports2026-10-12

Presumed hepatic pseudolipoma detected as a small hepatic surface lesion: multimodality imaging findings.

Soga Koichi K, Takagi Ou O, Inaba Kohei K, Masuda Mikako M et al.

Hepatic pseudolipomas are uncommon benign lesions located on or near the liver capsule which are thought to arise from a detached epiploic appendage that becomes trapped near Glisson's capsule. Because these lesions may appear as small hepatic or perihepatic nodules, they can mimic primary or metastatic hepatic tumors on screening imaging. Here, we report the case of a 55-year-old asymptomatic man with no relevant medical history who was referred after routine health-screening ultrasonography revealed a 10 × 8-mm hyperechoic lesion adjacent to the surface of liver segment VI. Liver function tests were normal, hepatitis B and C viral markers were negative, and tumor markers, including carcinoembryonic antigen, carbohydrate antigen 19-9, alpha-fetoprotein, and protein induced by vitamin K absence or antagonist-II, were within the normal ranges. Dynamic ultrasonography demonstrated that the lesion was located along the hepatic capsule, rather than within the deep hepatic parenchyma. Computed tomography showed a well-demarcated hepatic surface lesion with central calcification and surrounding fat attenuation, without any arterial, portal venous, or delayed enhancement. Gadoxetate disodium-enhanced magnetic resonance imaging revealed fat-containing signal characteristics, no hepatobiliary-phase uptake, and no diffusion restriction. The integrated multimodal imaging findings supported a diagnosis of presumed hepatic pseudolipoma, likely originating from a detached epiploic appendage. Recognition of this benign hepatic tumor mimic may help to avoid unnecessary biopsy or surgery.

PMID 42861266
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PubMedbioRxiv : the preprint server for biology2026-10-11

Depletion of border-associated macrophages impairs CSF flow and exacerbates extranuclear mutant Huntingtin aggregation in the zQ175DN mouse model of Huntington's disease.

Jiang Yanli Y, Sondawle Rahul R, Moniz Helen H, Mu Emily E et al.

Huntington's disease (HD) is a fatal, neurodegenerative disorder driven by a CAG trinucleotide repeat expansion in the huntingtin ( HTT ) gene, resulting in neuronal toxicity and brain atrophy, initially in the most vulnerable brain region striatum and expanding to the cortex and other brain regions along disease progression. While cell-autonomous mechanisms within neurons have been extensively characterized, how brain waste clearance pathways at the brain's borders change during disease progression remains poorly understood. In this study, we investigated the structural and functional adaptations of border-associated macrophages (BAMs) in the zQ175DN knock-in mouse model of HD. Immunohistochemical analysis revealed an age-dependent, selective reduction in the CD206 + Lyve1 + subset of leptomeningeal BAMs in 16-month-old zQ175DN mice, which tightly correlated with a profound impairment in cerebrospinal fluid (CSF) flow velocity and perivascular influx. To determine whether BAMs actively drives this CSF flow, we selectively depleted these populations of macrophages in 10-month-old zQ175DN mice via intracerebroventricular (i.c.v.) injection of clodronate liposomes (CLO). Chemical ablation of BAMs significantly exacerbated global CSF dynamic impairment, indicted by decreasing CSF fluorescent tracer distribution across perivascular parenchymal channels. Crucially, this CSF flow failure resulted in a marked accumulation of extranuclear mutant huntingtin (mHTT) aggregates in the zQ175DN HD mouse brain, while intranuclear inclusions were not significantly altered. Furthermore, BAMs depletion did not alter microglial or astrocytic gliosis in the brain, demonstrating that the exacerbation of mHTT load is a byproduct of brain waste clearance dysfunction. Together, our results indicate that BAMs are non-redundant regulators of CSF flow dynamics at the brain borders, offering a unique non-neuronal therapeutic target to combat HD. Age-dependent reduction of specific CD206 + Lyve1 + border macrophages (BAMs) occurs in HD mice. Ablation of BAMs significantly restricts CSF flow in HD mice.BAMs depletion selectively exacerbates extranuclear mHTT accumulation in HD mice.mHTT clearance failure induced by BAMs depletion occurs independently of gliosis.

PMID 42856241
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PubMedNeurochemical research2026-10-08

Maresin1 Improves Angiogenesis and Cognitive Function by Regulating Perivascular Macrophages in Rats with Chronic Cerebral Hypoperfusion.

Song Hao H, Du Miaoyu M, He Haoying H, Zhang Ran R et al.

Population aging imposes a substantial dementia burden. Chronic cerebral hypoperfusion (CCH) serves as a crucial early pathological basis for Alzheimer's disease (AD) and Vascular Dementia (VaD). Our previous studies have demonstrated that macrophage-derived docosahexaenoic acid metabolite Maresin1 can ameliorate CCH-induced cognitive impairment, though the underlying angiogenesis-related mechanisms remain to be elucidated. We developed a rat model of chronic cerebral hypoperfusion using the bilateral common carotid artery occlusion surgical approach. Cognitive improvements and angiogenic mechanisms by Maresin1 were systematically evaluated using behavioral assessments, immunofluorescence techniques, Western blotting (WB), ELISA, and cerebral blood flow measurements via laser Doppler. Our findings revealed that Maresin1 administration significantly ameliorated CCH-induced cognitive deficits, promoted hippocampal angiogenesis and enhanced cerebral perfusion. Further analysis showed significant enhancement of IGF-1/p-Akt/VEGF/eNOS signaling pathway activation by Maresin1, and the increased VEGF expression was predominantly mediated by perivascular macrophage (pvMΦ) activation. Depletion of pvMΦ using clodronate liposomes suppressed the VEGF upregulation and cognitive improvement mediated by Maresin1. Our research demonstrates that IGF-1/p-Akt/VEGF pathway activation in pvMΦ plays a crucial role in Maresin1-mediated angiogenesis in CCH rats.

PMID 42848243
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