Drug Database
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

PubMedBiomolecules2026-08-27

Selective Pharmacological Activation of PPARα/δ/γ Alters the Triglyceride Composition of Fatty Liver in a Diet-Induced MASLD Mouse Model.

Hishiki Takako T, Honda Akihiro A, Tanaka Reina R, Minomo Yukiko Y et al.

Various high-fat diets have been used to create animal models of metabolic dysfunction-associated steatotic liver disease (MASLD) and to evaluate the effect of various therapeutic drugs. We determined the effects of PPARα/δ/γ subtype-selective agonists (pemafibrate, seladelpar, and pioglitazone, respectively) on the hepatic triglyceride (TG) profile using LC-MS in a MASLD mouse model established by administering a high-fat/high-cholesterol/high-cholic acid (HFCC) diet combined with cyclodextrin-containing water, which is thought to induce fatty liver over a short period. The livers of mice fed the HFCC/CDX diet for four weeks exhibited an approximately fivefold increase in the summed TG LC-MS signal per unit liver weight and altered TG composition compared with normal livers of mice administered a standard diet/water. Specifically, the proportion of TG54 (TG with 54 carbon atoms) species doubled, whereas the proportion of TG52 decreased by 38%. Pemafibrate did not alter the relative total TG signal but decreased the proportion of some TG58/TG56 species and increased the proportion of some TG56/TG52 species. Seladelpar did not alter the relative total TG signal, while only slightly altering TG composition. Pioglitazone reduced the relative total TG signal by 44%, which included a decrease in the proportion of polyunsaturated fatty acid-rich TG54 and an increase in the proportion of TG58/TG56 with 1-3 unsaturated bonds. We are the first to demonstrate that selective activation of PPARα/δ/γ has different effects on the TG profile in fatty liver.

PMID 42650746
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PubMedCell biochemistry and biophysics2026-08-22

Host-Derived Proteomic Profiling of Human and Canine Mammary Tumor Xenografts Identifies Enrichment of Lipid Metabolism-Related Pathways.

Díaz-Grijuela Elisa E, Goñi Saioa S, Urdiciain Alejandro A, Barajas Miguel M et al.

Breast cancer is the most frequently diagnosed cancer in women worldwide and one of the most common malignancies in dogs. Notable clinical, hormonal and molecular similarities between both species suggest that dogs may serve as a valuable comparative oncology model. Alterations in lipid homeostasis and metabolism are closely associated with the acquisition of cancer hallmarks. In this study, a comparative proteomic analysis of murine host-derived proteins was performed in cell line-derived xenograft (CDX) models generated from human triple-negative breast cancer cell line (MDA-MB-231) and a canine mammary carcinoma cell line (CMT-U27). Using LC-MS/MS and species-resolved proteomics, tumor-associated changes in the host proteome were characterized across models. In total, 577 proteins were differentially identified in tumor tissues compared with healthy mammary gland samples in this interspecies CDX comparison, with 51.99% showing increased and 46.79% decreased relative abundance, while a small proportion displayed opposite regulation patterns between models. Functional enrichment analysis revealed that several biological processes were altered, including pathways related to lipid metabolism. Moreover, proteins involved in lipid pathways showed a moderate level of concordance between models (r > 0.6, Mann-Whitney U test p < 0.05). Overall, these findings provide a descriptive overview of host-derived proteomic alterations in interspecies mammary tumor CDX models and suggest that lipid metabolism-related pathways may be involved in tumor-associated microenvironmental changes. This study should be considered exploratory and hypothesis-generating, providing a basis for future studies incorporating orthogonal validation and controlled experimental designs.

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PubMedRare tumors2026-08-22

Pulmonary carcinoid harboring a KRAS G12C mutation identified through comprehensive genomic profiling and responding to sotorasib: A case report.

Hamai Kosuke K, Abe Masaaki M, Miyake Shinya S, Katsura Ryo R et al.

Pulmonary carcinoids are the pulmonary counterparts of gastrointestinal neuroendocrine tumors (NETs) G1-2. They may cause distant metastasis, leading to a poor prognosis, and requiring chemotherapy. Reports on cases harboring driver gene mutations remain limited. A man in his late 60s visited to JA Onomichi General Hospital because he was suspected of lung cancer. Positron emission tomography/computed tomography (PET/CT) showed a 24-mm nodule in the right upper lobe with abnormal ^18F-fluorodeoxyglucose uptake, and bronchoscopic examination revealed adenocarcinoma. Surgery was planned for stage IA3 lung adenocarcinoma; however, intraoperative findings demonstrated pleural dissemination, and the procedure was terminated as an exploratory thoracotomy. Pathological examination of tissue obtained from the pleural dissemination showed features consistent with NET G2, confirming a diagnosis of atypical carcinoid. Ten months after treatment with carboplatin plus etoposide, salvage surgery consisting of right upper lobectomy and resection of pleural dissemination was performed. Histopathological examination revealed a papillary adenocarcinoma adjacent to a NET G2. Three months after surgery, CT revealed a metastatic lesion in the retrohepatic segment. Histological examination of the liver tumor obtained via laparoscopic hepatectomy confirmed a NET G2 without adenocarcinomatous components. Four months after hepatectomy, PET/CT demonstrated multiple lymph node metastases. The patient was treated sequentially with carboplatin plus etoposide, everolimus, and amrubicin, however, the liver metastases progressed. A liver tumor biopsy was performed for comprehensive genomic profiling (CGP). The biopsy specimen revealed metastatic NET G2. FoundationOne CDx testing identified KRAS G12C mutation, and treatment with sotorasib was initiated. One year has passed since the initiation of sotorasib with no serious adverse events. The liver metastases have regressed, and tumor marker levels have decreased. Sotorasib is effective for treating KRAS G12C-positive pulmonary carcinoids. Because pulmonary NETs rarely harbor driver mutations, CGP testing may be considered.

PMID 42630346
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PubMedbioRxiv : the preprint server for biology2026-08-20

Breast cancer ovarian metastases show increased activity of GPCR pathways.

Savariau Laura L, Qin Ye Y, Shah Osama O, Basudan Ahmed M AM et al.

Treatment resistance and metastases occur in 10-20% of patients with invasive lobular carcinoma (ILC), the most common special histological subtype of breast cancer. ILC metastasizes to the ovary more frequently than no special type (NST) tumors, also known as invasive ductal carcinoma (IDC). To characterize the genomic landscape of breast cancer ovarian metastases, we analyzed 15,613 local breast cancers, 22,010 non-ovarian metastases, and 246 ovarian metastases sequenced using FoundationOne®CDx or FoundationOne® assays. Ovarian metastases had enriched CDH1, PIK3CA, and TBX3 mutations and depleted TP53 and MYC alterations relative to local breast cancers, with additional depletion of ESR1 mutations compared to non-ovarian metastases. CDH1 mutations were less frequent in ovarian metastases (47%) than local ILC (81.3%), with reduced 16q loss (64% vs 84%), indicating that ovarian metastases also arise from non-ILC tumors. We extended these findings to a UPMC cohort of 27 ovarian metastases (13 ILC, 8 IDC, 6 mixed ductal-lobular carcinoma) with patient-matched primary tumors in most cases. In both cohorts, patients with ovarian metastases were significantly younger than those with other metastatic sites. In the UPMC cohort, the most frequent mutations were in PIK3CA, CDH1, KMT2C, FOXA1, and RUNX1. Transcriptomic analysis identified upregulated G protein-coupled receptor (GPCR) pathways, including metabotropic glutamate receptor signaling. Functional studies showed that calcium-sensing receptor (CaSR), a GPCR overexpressed in ovarian metastases, drives MEK/ERK-dependent migration and F-actin reorganization in ILC cell lines, enhanced by estrogen and blocked by calcilytic, MEK, or anti-estrogen treatment. Our findings inform future therapeutic targeting of ovarian metastasis.

PMID 42619866
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PubMedFrontiers in oncology2026-08-19

Targeting MEST using cobicistat as a therapeutic strategy for gastric cancer through suppressing NF-κB signaling.

Cao Hongtai H, Ye Huili H, Zhang Wentao W, Cai Weiwen W et al.

Gastric cancer (GC) constitutes a substantial global public health challenge, and the lack of tractable molecular targets limits therapeutic progress. Mesoderm-Specific Transcript (MEST) has been implicated in tumor-related signaling, yet its functional role and druggability in GC remain undefined. The analyses of GC tissue microarrays and cohorts were performed to evaluate MEST expression and its clinical significance. CRISPR/Cas9-mediated MEST knockout was used to characterize its oncogenic functions in GC cells and xenograft models. Integrated RNA sequencing and pathway analysis was utilized to elucidate signaling pathways under the regulation of MEST. A structure-guided virtual screen combined with SPR binding and phenotypic assays were employed to discover small molecules targeting MEST. The therapeutic effects and mechanism of the lead compound were evaluated using GC cell lines, patient-derived organoids, cell-derived xenograft (CDX), and patient-derived xenograft (PDX) models. MEST expression in GC tissues was elevated and linked to poor prognosis. Functionally, genetic ablation of MEST impaired GC cell proliferation, invasion, migration, and suppressed tumor growth in CDX models. Screening of approved-compound libraries identified cobicistat as a previously unrecognized high-affinity candidate MEST-inhibitory compound. Cobicistat suppressed tumor growth across a panel of preclinical GC models, including cell lines, organoids, CDX and PDX. Mechanistically, MEST may drive GC progression by activating the NF-κB pathway, whereas cobicistat may antagonize MEST binding and blocked NF-κB pathway. MEST functions as a key oncoprotein driving GC progression via NF-κB activation. Cobicistat, a candidate MEST-inhibitory compound, exhibits favorable preclinical efficacy and safety, providing a promising candidate for targeted GC therapy.

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PubMedJournal of visualized experiments : JoVE2026-08-19

Standardized Xenograft Models for Preclinical Cancer Research.

Ovcharenko Dmitriy D

Xenograft models are the principal in vivo platform of preclinical oncology and the most established experimental link between cell culture and clinical investigation. From the carcinogen-exposed rabbit models of the early twentieth century through the current generation of humanized patient-derived xenograft (PDX) systems, these platforms have evolved in response to the demands of translational cancer research. This review critically examines the biological principles, methodological standards, and translational applications of the principal xenograft platforms in current use. Cell line-derived xenograft (CDX) models remain the most widely used and most cost-effective modality for preclinical efficacy testing, offering the reproducibility, scalability, and accessibility that have sustained their role across oncology drug development pipelines for decades. PDX models have emerged as the preferred platform for co-clinical trial design, predictive biomarker discovery, and personalized oncology applications, preserving the genomic landscape, intratumor heterogeneity, and histological architecture of the donor tumor across serial passages. The engraftment biology of PDX systems, including immunodeficient host strain selection, implantation site, tumor source, and passage biology, is reviewed, together with humanized and autologous humanized configurations that extend the platform to immune checkpoint inhibitors, bispecific T-cell engagers, and chimeric antigen receptor T (CAR-T) cell therapy evaluation. This review addresses preclinical-to-clinical translation as a function of immunological divergence, incomplete tumor microenvironment recapitulation, and standardization. Formal frameworks, including the PDX Model Minimal Information (PDX-MI) standard and the Minimal Information for Standardization of Humanized Mice (MISHUM), are examined alongside global biobank infrastructure and emerging AI-driven translational modeling approaches.

PMID 42615474
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