P3, N=114, Active, not recruiting, Westmead Hospital Research and Education Network | Not yet recruiting --> Active, not recruiting

This first comprehensive FAERS study identifies key drugs associated with ILI, including interferon β-1a, evolocumab, ofatumumab, interferon β-1b, and zoledronic acid. Clinical monitoring for drug-induced ILI is essential to enhance medication safety.

P1/2, N=30, Not yet recruiting, Assistance Publique Hopitaux De Paris

The patient was treated with vinblastine and prednisolone, along with desmopressin and somatotropin replacement. Zoledronic acid was added for osseous disease...This case highlights an unusual presentation of adult LCH with distal lower-extremity and tarsal bone involvement, as well as hypothalamic-pituitary disease preceding osseous diagnosis by two years. It underscores the importance of considering LCH in adults with unexplained multifocal lytic bone lesions and endocrine dysfunction, and it demonstrates that durable disease control can be achieved with systemic therapy.

Peripheral blood monocyte-derived macrophages in mice were depleted through intraperitoneal administration of clodronate liposomes...Our findings demonstrated that TNFAIP3 in macrophages modulates subretinal fibrosis of CNV lesions by regulating M2 polarization through the NF-κB/Spi1/C/EBPβ signaling pathway. These results suggest that targeting TNFAIP3 in M2 macrophages might serve as a promising therapeutic strategy for CNV and subretinal fibrosis.

These findings suggest that miR-466f-3p regulates innate immunity by promoting pro-inflammatory activation of macrophages and contributes to the suppression of metastasis. iPS-EVs represent a promising platform for EV-based immunotherapy targeting innate immune reprogramming to suppress cancer metastasis.

We established a novel metabolic vulnerability in hormone-responsive malignancies. These findings position ZA as a bifunctional ferroptosis inducer in ER+ breast cancer, offering a promising strategy to overcome endocrine resistance.

P4, N=100, Recruiting, Hospital for Special Surgery, New York | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

CoQ deficiency disrupts oxidative phosphorylation (OXPHOS) and pyrimidine metabolism, causes mitochondrial ROS accumulation, induces mitochondrial antiviral protein (MAVS) oligomerization, and activates the pyrin inflammasome. This mevalonate-CoQ-OXPHOS/pyrimidine metabolism axis serves as a promising target for screening additional immune-metabolic adjuvants, and nanofabrication offers a paradigm for the lymph-targeted in vivo delivery of such adjuvants.

Its function was investigated through small interfering RNA-mediated silencing, lentiviral overexpression, pamidronate treatment, in vitro proliferation, migration, invasion, and apoptosis assays, xenograft models, phosphoproteomic profiling, and Western blot validation. FDPS knockdown was further associated with decreased B-cell lymphoma 2 expression, reduced phosphorylation of Caspase-9 at Ser196, increased cleaved Caspase-3, and reduced phosphorylation of mechanistic target of rapamycin at Ser2448. Collectively, these findings suggest that FDPS contributes to HCC progression and may serve as a candidate biomarker and therapeutic target.

Despite intensive treatment with intravenous hydration and zoledronic acid, neurological deterioration occurred; hence, after 25 days of hospitalization, the patient was discharged for home-based palliative care at the family's request. This case highlights the importance of considering metastatic malignancies, particularly breast cancer, in patients with pancreatitis of unclear etiology and severe hypercalcemia.

Romiplostim-induced MF in a mouse model demonstrated extensive bone marrow (BM) CHI3L1 mRNA expression, which was reversed by clodronate treatment. A culture assay revealed that high CHI3L1 concentrations promoted extracellular matrix production by fibroblast cell lines, and that a CHI3L1-neutralizing antibody abrogated this effect. These results indicate the importance of CHI3L1 in the association between fibrocytes and fibroblasts in MF and could be a focus for future treatment.