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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

PubMedTranslational oncology2026-11-10

Analytical and clinical validation of Ion Torrent™ Oncomine™ Dx Express Test for identifying PIK3CA/AKT1/PTEN-altered tumors in patients with hormone receptor-positive advanced breast cancer for treatment with capivasertib.

Elvidge Charlotte C, Heung Macy M, Clark Thomas T, Egile Coumaran C et al.

This study reports on analytical and clinical validation of the highly automated Ion Torrent™ Oncomine™ Dx Express Test (ODxET) for detecting PIK3CA/AKT1/PTEN-altered tumors in patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative advanced or metastatic breast cancer that may benefit from treatment with capivasertib plus fulvestrant. Analytical validation studies were completed using commercially sourced breast cancer tissue specimens to establish the ODxET assay detection capability (limit of detection, limit of blank), precision (repeatability, reproducibility), and effect of endogenous interfering substances for detecting PIK3CA/AKT1/PTEN alterations. Clinical validation was performed using 429 residual breast cancer tissue samples from the Phase 3 CAPItello-291 trial and progression-free survival (PFS) was analyzed for patients with PIK3CA/AKT1/PTEN-altered tumors, as detected by ODxET, and compared to efficacy outcomes from the CAPItello-291 study. Comparison of assay agreement between ODxET and FoundationOne®CDx (F1CDx) gave an overall, positive and negative percent agreement of 89.2%, 82.0%, and 96.6%, respectively. The 18% false negative rate observed with ODxET was largely attributable to limited detection of complex PTEN variants. PFS benefit was observed with capivasertib plus fulvestrant versus placebo plus fulvestrant in patients with PIK3CA/AKT1/PTEN-altered tumors detected by ODxET (n=162; hazard ratio 0.55, 95% confidence interval [CI]: 0.38-0.78). This is similar to the observed PFS benefit in the population with PIK3CA/AKT1/PTEN-altered tumors identified by F1CDx in the CAPItello-291 trial (hazard ratio 0.49, 95% CI: 0.38-0.64). This study demonstrates the clinical utility of ODxET to identify patients with PIK3CA/AKT1/PTEN-altered tumors that may benefit from treatment with capivasertib plus fulvestrant.

PMID 43008349
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PubMedJournal of pharmaceutical analysis2026-11-08

Cyclovirobuxine D suppresses gastric cancer growth by targeting the V-ATPase complex and inducing excessive endo-lysophagy.

Li Chongyang C, Xu Minghao M, Ji Yacong Y, Deng Chaowei C et al.

Gastric cancer is one of the most malignant cancers in the world, posing a significant threat to human life and persisting as a major clinical challenge. Cyclovirobuxine D (CVB-D), derived from boxwood and traditionally employed in cardiovascular disease treatment, has emerged as a promising candidate for cancer therapy. However, its mechanism of action still needs to be clearly defined. We aimed to comprehensively evaluate CVB-D's impact on gastric cancer and elucidate its underlying mechanisms. Here, we found CVB-D induced excessive endo-lysophagy in gastric cancer. Moreover, subsequent experimental analyses revealed that CVB-D directly engages the ATPase H+ transporting V0 subunit a1 (ATP6V0A1)-containing V-ATPase complex and perturbs endo-lysosomal homeostasis, leading to abnormal lysosomal acidification, impaired lysosomal protease activity, and autophagic flux blockade. Mechanistically, damaged endo-lysosomes recruited the autophagic adaptor P62/sequestosome 1 (SQSTM1) in a galectin8 (Gal8)-dependent manner, ultimately triggering endoplasmic reticulum (ER) stress and apoptosis in gastric cancer cells. Furthermore, through cell-derived xenograft (CDX) and patient-derived xenograft (PDX) models, we validated the therapeutic efficacy of CVB-D against gastric cancer. Notably, CVB-D enhances the sensitivity of gastric cancer to the chemotherapeutic agent cisplatin. Our findings suggest that CVB-D holds promise as an effective therapeutic agent for gastric cancer treatment.

PMID 42997595
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PubMedOncotarget2026-11-05

Assessment of genomic instability and homologous recombination repair in ovarian cancer using the Oncomine Comprehensive Assay Plus.

Goetting Isabell I, Rau Achim A, Russ Luisa L, Kommoss Stefan S et al.

Copyright: © 2026 Goetting et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Homologous recombination deficiency (HRD) is associated with response to poly (ADP-ribose) polymerase inhibitors (PARPi) in ovarian cancer and can be assessed through BRCA1/2 loss-of-function alterations and overall genomic instability. HRD status was characterized in 58 ovarian cancer samples, primarily high-grade serous ovarian carcinoma (HGSC, n = 52), using the Oncomine™ Comprehensive Assay (OCA) Plus. HRD status was determined based on BRCA1/2 variants and a genomic instability metric (GIM) and compared with the FDA-approved gold standard method MyChoice® CDx assay. Overall, 33 samples (56.9%) were HRD-positive, including 53.4% of HGSC samples. BRCA1/2 mutations were detected in 11 samples (19.0%), with BRCA1 more frequently affected. Concordance between OCA Plus and MyChoice CDx assays was 91.4% for BRCA1/2 alterations, 83.3% for GIM, and 86.0% for HRD classification. Additional alterations of potential clinical relevance such as variants in homologous recombination repair genes, including ATM, PTEN, FANCE, and CDK12, CCNE1 amplifications, and TP53 mutations (86.2%) were detected. Loss of heterozygosity in BRCA1/2-mutated samples suggested potential biallelic loss-of-function. HRD-positive tumors, including both BRCA1/2-mutated and BRCA-wild type cases, showed significantly longer recurrence-free survival and apparent clinical benefit from PARPi treatment. This study supports the feasibility of in-house HRD assessment using comprehensive genomic profiling panels for precise molecular characterization.

PMID 42985963
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PubMedVirchows Archiv : an international journal of pathology2026-11-05

A patient with Lynch syndrome and duodenal neuroendocrine carcinoma achieved a pathologic complete response to immune checkpoint inhibitor therapy selected based on comprehensive genomic profiling.

Sano Tomoya T, Ohira Go G, Maeda Kiyoshi K, Kohashi Kenichi K et al.

We report a 27-year-old man with stage IV duodenal neuroendocrine carcinoma (NEC) harboring microsatellite instability-high (MSI-H) and high tumor mutational burden (TMB-high) status, who achieved a pathologic complete response to pembrolizumab selected based on comprehensive genomic profiling (CGP). After failure of platinum-based chemotherapy, CGP using FoundationOne CDx revealed MSI-H, TMB-high, and a pathogenic MSH2 frameshift variant, prompting second-line pembrolizumab, which produced marked tumor regression and enabled pancreaticoduodenectomy. The resected specimen showed no viable tumor in the primary lesion or lymph nodes, confirming a pathologic complete response; the patient has remained recurrence-free for 3 years. Germline testing confirmed the same MSH2 variant, establishing a diagnosis of Lynch syndrome; cascade testing identified four carrier relatives and enabled early detection of gastric cancer in a 24-year-old carrier. Duodenal NEC associated with Lynch syndrome has not been previously reported. This case illustrates the diagnostic and therapeutic value of CGP in rare gastrointestinal NEC.

PMID 42983056
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PubMedCancer science2026-11-04

Landscape and Time Course of Comprehensive Genomic Profiling Use in Japanese Patients With Cancer: A Retrospective Study.

Sunami Kuniko K, Mikami Masashi M, Tanaka Masayuki M, Aoyagi Sona-Sanae SS et al.

Comprehensive genomic profiling (CGP) is standard for advanced solid tumors. Evidence reporting its real-world utilization pattern and time course for guided therapy is limited. This retrospective study in Japan assessed the real-world utility of CGP tests for advanced or metastatic solid tumors using data from the C-CAT registry from June 1, 2019, to August 23, 2025. We evaluated the proportion of patients who received genomically matched therapy with expert panel (EP) recommendation and their overall survival (OS) compared with patients who did not receive genomically matched therapy. The study population comprised 89,552 patients who underwent CGP: median age 64.0 (interquartile range: 54.0-72.0) years, with pancreatic cancer (13,827; 15.4%) and colorectal cancer (11,322; 12.6%) the most common tumor types. System-generated matched treatment options presented as reference information during EP review were identified in 80,185, of whom 77,337 (96.4%) received EP review, 37,245 (46.4%) were offered new therapeutic recommendations, and 7124 (8.9%) initiated EP-recommended therapies. Among 2049 patients who were newly identified with companion diagnostic (CDx)-related druggable alterations, 319 (15.6%) received matched therapies. Patients receiving matched therapies experienced longer OS compared with others in the overall cohort (median: 538 days vs. 356 days) and across cancer types. OS varied by the final treatment line before CGP testing, with earlier lines associated with longer survival in biliary tract, ovarian, pancreatic, and thyroid cancers. These findings highlight the need for timely CGP implementation to maximize the impact of precision oncology. Trial Registration: Japan Registry of Clinical Trials identifier: jRCT1030250365.

PMID 42978394
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PubMedBiochemical pharmacology2026-11-04

A recombinant CD99-targeted antibody-drug conjugate for Ewing sarcoma therapy.

Sabapathy Yogalakshmi Y, Ramachandran Balaji B, Ramanathan Priya P, Sundersingh Shirley S et al.

Ewing sarcoma (ES) is an aggressive paediatric malignancy characterised by high CD99 expression and limited targeted therapeutic options. In this study, we developed a recombinant anti-CD99 Cancer Institute Antibody (CIAb-anti-CD99) by isotype switching a hybridoma-derived IgM/κ antibody to an IgG2a/κ format to improve manufacturability and therapeutic applicability. Recombinant CIAb-anti-CD99 was expressed in CHO-K1 cells and retained specific recognition of CD99, as demonstrated by immunofluorescence, flow cytometry, Western blotting, and immunohistochemistry. Functionally, CIAb-anti-CD99 increased the Annexin V/PI-positive cell population and inhibited proliferation and clonogenic growth of CD99-positive ES cells in vitro. To evaluate the potential of CIAb-anti-CD99 for targeted drug delivery, CIAb-anti-CD99 was conjugated to doxorubicin to generate a CD99-targeted antibody-drug conjugate (CIAb-Dox). In vivo biodistribution studies demonstrated tumour localisation and prolonged retention of CIAb-anti-CD99 in A673 xenograft tumours. Therapeutic evaluation in an A673 cell line-derived xenograft (CDX) model showed that CIAb-Dox significantly suppressed tumour growth compared with vehicle and antibody monotherapy. Histopathological analysis demonstrated lower viable tumour content and greater tumour necrosis in CIAb-Dox-treated tumours. Quantitative immunohistochemical analysis further showed a significant reduction in the Ki67-positive proliferative index and increased cleaved PARP staining, consistent with apoptosis-associated cellular changes. CIAb-Dox demonstrated enhanced antitumour activity while maintaining a favourable tolerability profile. Collectively, these findings provide preclinical evidence supporting further investigation of CD99-directed antibody-drug conjugates. CIAb-anti-CD99 represents a functionally active CD99-targeting antibody, while CIAb-Dox warrants further evaluation in additional Ewing sarcoma models, together with mechanistic, pharmacokinetic, and comprehensive analytical studies.

PMID 42982199
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