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TL

TLX007-CDx (TLX007 CDx / TLX007CDx)

✓ Approved

Telix Pharmaceuticals Limited · Imaging Agents · Imaging Agents

What is TLX007-CDx?

TLX007-CDx is a imaging agents developed by Telix Pharmaceuticals Limited. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesTLX007 CDx, TLX007CDx
CompanyTelix Pharmaceuticals Limited
Drug ClassImaging Agents
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Telix Pharmaceuticals Limited

Therapeutic Indications

TLX007-CDx is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Prostate cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancerBLA/NDA

Related Research Articles

PubMedPancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]2026-07-24

Clinical characteristics and therapeutic implications of MTAP deletion in pancreatic cancer: A nationwide genomic analysis.

Matsumoto Hiroya H, Mizuno Kazuyuki K, Kondo Chiaki C, Kawashima Hiroki H et al.

Methylthioadenosine phosphorylase (MTAP) deletion is a frequent genomic alteration in several cancers and a potential therapeutic vulnerability. However, its prevalence and clinical significance in pancreatic cancer remain insufficiently characterized. We retrospectively analyzed 8834 patients with pancreatic cancer profiled by FoundationOne® CDx in a nationwide genomic cohort. MTAP-deleted and non-deleted groups were compared for clinicopathological characteristics, co-occurring genomic alterations, tumor mutational burden (TMB), microsatellite instability (MSI), overall survival (OS), and treatment response to first- and second-line chemotherapies. MTAP deletion was identified in 27.3% of pancreatic cancers, with high frequencies in pancreatic ductal adenocarcinoma (PDAC) (28.0%) and adenosquamous carcinoma (35.0%). MTAP deletion strongly co-occurred with CDKN2A/2B deletion and was associated with major driver alterations (KRAS, TP53, SMAD4), while showing no association with high TMB or MSI. In PDAC, the median OS was significantly shorter in the MTAP-deleted group compared with the non-deleted group (24.3 vs. 29.9 months; P < 0.0001). However, CDKN2A-deleted subcohort analysis revealed that MTAP deletion was not associated with OS (HR: 0.96; 95% CI: 0.85-1.08). Furthermore, the objective response and disease control rates to gemcitabine plus nab-paclitaxel or FOLFIRINOX were comparable between the groups. MTAP deletion is a frequent genomic alteration in pancreatic cancer. Although it was not an independent prognostic or chemotherapy-predictive biomarker, our comprehensive clinicogenomic findings provide a foundation for future evaluation of MTAP-focused therapeutic strategies in pancreatic cancer.

PMID 42493328
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PubMedFrontiers in oncology2026-07-23

Case Report: extensive leptomeningeal metastasis from gastric cancer presenting with hearing impairment.

Lin Yan-Cheng YC, Li Xiang X, Zhan Xi-Chang XC, Dong Wan-Hui WH

Leptomeningeal metastasis (LM) from gastric cancer is a rare but devastating manifestation of advanced disease. Early diagnosis can be difficult when neurological symptoms are atypical and cerebrospinal fluid (CSF) cytology is negative. We report a 71-year-old man with gastric cardia adenocarcinoma who initially developed hearing impairment, dizziness and gait instability approximately 11 months after radical total gastrectomy, followed by rapidly progressive bilateral hearing loss at presentation. Neurological examination initially showed no meningeal signs or pathological reflexes. Contrast-enhanced brain magnetic resonance imaging (MRI) demonstrated extensive, multifocal linear and patchy leptomeningeal enhancement over the bilateral cerebral hemispheres and cerebellar surfaces. CSF analysis showed marked hypoglycorrhachia, elevated protein, and mild mononuclear pleocytosis, whereas cytology did not identify malignant cells. After alternative infectious and immune-related diagnoses were considered clinically less likely, the findings supported a diagnosis of probable type IIA LM according to the EANO-ESMO criteria. Immunohistochemistry of the primary gastric tumor showed CK7 positivity, diffuse CAM5.2 positivity, partial CDX-2 nuclear positivity, HER2 immunohistochemistry (IHC) 2+ membranous staining, mutant-pattern p53 expression, and a Ki-67 proliferation index of approximately 90%. The disease progressed rapidly to impaired consciousness, and the family chose best supportive care after a multidisciplinary team (MDT) discussion. This case highlights that leptomeningeal metastasis from gastric cancer may initially present with hearing impairment; integrated assessment of MRI findings, CSF biochemistry, clinical course, and careful consideration of alternative diagnoses is essential.

PMID 42488117
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PubMedEJNMMI research2026-07-22

Preclinical PET characterization of [68Ga]Ga-EMP-100 for non-invasive assessment of c-Met in NSCLC.

Rusu Timofei T, Rodenas Anita A, Capet Leo L, Perrier Alexandre A et al.

The c-Met receptor is a key therapeutic target in non-small cell lung cancer (NSCLC). Current methods for assessing c-Met level, are limited by biopsy sampling, which fails to account for spatio-temporal and intra-tumour heterogeneity. This study aims to evaluate the use of PET/CT imaging for non-invasive, full-body quantification of c-Met expression in different subtypes of NSCLC, encompassing both ADC and squamous cell carcinoma and compare it to MET gene alterations and IHC c-Met scoring. [68Ga]Ga-EMP-100, a PET radiotracer targeting c-Met, was radiolabelled and characterized. Cell-Derived Xenograft (CDX) models of NSCLC with different characteristics were developed and validated for PET/CT imaging using [68Ga]Ga-EMP-100. Tumour uptake and heterogeneity were quantified and compared to c-Met expression determined by IHC (H-score using SP44 and EP1454Y antibodies) and MET gene amplification detected by FISH and NGS. Automated radiolabelling of [68Ga]Ga-EMP-100 demonstrated a high radiochemical yield (RCY) and purity (RP). Pharmacokinetics studies revealed rapid excretion predominantly by the renal pathway. PET/CT imaging resulted in high contrast and enabled non-invasive classification of CDX models regarding c-Met receptor levels. The highest tumour uptake was observed in H1648 and EBC-1 models. Although MET gene alterations were not correlated with c-Met protein expression at the cell surface, a good correlation was found between SUVmax and c-Met expression, when using the EP1454Y antibody. PET/CT imaging using [68Ga]Ga-EMP-100 successfully quantified c-Met expression in vivo, clearly adding up to conventional IHC and genetic methods. Our study adds novel comparative evidence across tumour histotypes, providing new insight into how tumour phenotype affects c-Met-targeted imaging. This radiotracer holds potential as a non-invasive tool for selecting patients for c-Met-targeted therapies and monitoring therapeutic response in NSCLC. Further clinical studies are warranted.

PMID 42481881
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PubMedAdvanced healthcare materials2026-07-21

A Triple-Stage Precision Carbon Dot Nanogel With Cascade Activation for Spatiotemporally Controlled Chemo-Photodynamic Therapy.

Zhang Yunxiao Y, Li Jianwei J, Yue Lei L, Zhang Changyu C et al.

Conventional chemotherapy is limited by poor cellular uptake and low tumor selectivity, often requiring high systemic doses that increase off‑target toxicity. Here we report a triple‑stage precision nanogel (CDX@nano) in which carbon dots (CDs) serve as organelle‑targeted delivery vehicles. The nanogel is surface-functionalized with indomethacin for tumor‑specific homing and encapsulates CDs conjugated with doxorubicin (DOX) via glutathione-cleavable disulfide linkages. Upon near-infrared irradiation, the CDs generate singlet oxygen, triggering nanogel disassembly, and rapid drug release. The liberated CDs accumulate in mitochondria, elevating reactive oxygen species and disrupting redox homeostasis, while DOX translocates to the nucleus to induce DNA damage. This cascade-activated, dual-compartment assault integrates photodynamic and chemotherapeutic modalities. In vitro, CDX@nano reduced tumor cell viability to 8.5% upon irradiation, showing approximately 4.5‑fold greater potency than non-targeted controls. In vivo, it achieved over 85% tumor growth inhibition with minimal systemic toxicity. This triple-stage platform offers a promising strategy to overcome key barriers in cancer therapy.

PMID 42478518
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PubMedJournal of translational medicine2026-07-18

TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.

Ke Zhi-Yin ZY, Li Jie J, Zhong Liang L, Chen Shan S et al.

Acute myeloid leukemia (AML) has a poor prognosis due to high chemoresistance and recurrence. TRIM24, an E3 ubiquitin ligase, is oncogenic in solid tumors, but its role in AML and regulation of the oncoprotein p110 CUX1 remain unclear. We performed bioinformatic analysis to assess TRIM24 expression, prognosis, and protein-protein interactions. Functional studies used genetic manipulation and pharmacological inhibition in AML cells. Protein interactions were examined by Co-IP, IP-MS, and immunofluorescence. The stability and ubiquitination of p110 CUX1 were examined via CHX chase assays and ubiquitination profiling. The biological and therapeutic significance of the identified axis was validated using cell proliferation, apoptosis assays, drug sensitivity tests, and a CDX mouse model. TRIM24 is overexpressed in AML and predicts poor prognosis. TRIM24 promotes proliferation and inhibits apoptosis. Mechanistically, TRIM24 functions as a scaffold-like adaptor to recruit USP10 to deubiquitinate and stabilize p110 CUX1 via K48-linked ubiquitin chain cleavage. The TRIM24/USP10/p110 CUX1 axis activates the MAPK signaling pathway, with CUX1 regulating ERK transcription. TRIM24 overexpression enriches DNA repair pathways, conferring cytarabine resistance. Targeting TRIM24 genetically or with dTRIM24 sensitizes AML cells to cytarabine in vitro and in vivo. Our study reveals a novel non-canonical role of TRIM24 as a stabilizer of the p110 CUX1 oncoprotein by recruiting USP10. This TRIM24/USP10/p110 CUX1 axis is critical for AML progression, clinical prognosis, and chemoresistance, presenting a promising therapeutic target for AML treatment.

PMID 42469871
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PubMedCancer letters2026-07-16

3D epigenomic remodelling mediated by Foxa1 drives gemcitabine resistance in pancreatic cancer.

Wang Xuelong X, Cao Yizhi Y, Gu Jiangning J, Qi Tuoya T et al.

Gemcitabine remains a cornerstone treatment for pancreatic ductal adenocarcinoma (PDAC), yet the emergence of resistance constitutes a major clinical challenge with poorly understood epigenomic mechanisms. Here, we identified the pioneer transcription factor Foxa1 as a master regulator of gemcitabine resistance through multi-omics analysis. Mechanistically, Foxa1 drives widespread super-enhancer (SE) reprogramming and 3D genome remodelling in resistant cells, which coordinately activates the expression of key resistance genes, notably Rrm1 and Cdadc1. This is accompanied by increased chromatin accessibility, elevated H3K27ac enrichment at SEs, and enhanced Foxa1 binding at regulatory elements. Moreover, post-translational stabilization of Foxa1 via USP7-mediated deubiquitination sustains this epigenomic program. Genetic ablation of Foxa1 or specific SE regions near Rrm1 resensitizes resistant cells to gemcitabine. Building upon this mechanism, we demonstrate that bromodomain and extraterminal (BET) inhibitors, which disrupt SE function, potently reverse resistance. Notably, the clinical-stage BET inhibitor AZD5153, in combination with gemcitabine, achieves robust tumor suppression and overcomes resistance in cell-derived xenograft (CDX) models by dismantling the Foxa1-mediated resistant transcriptome and reinvigorating drug sensitivity. Our findings establish Foxa1-orchestrated enhancer reprogramming as a fundamental mechanism of gemcitabine resistance and unveil a promising epigenetic therapy to restore treatment efficacy in PDAC.

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