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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

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

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.

PubMedInternational journal of molecular sciences2026-07-15

Complete and Persistent Response to Immunotherapy in Highly Pretreated MSS TMB-High Pancreatic Adenocarcinoma: A Case Report and Literature Review.

Miceli Chiara Carmen CC, Caropreso Giuseppe G, Pacifico Giovanni G, Valletta Erika Lara EL et al.

Despite advances in precision medicine, therapeutic options for pancreatic adenocarcinomas are limited, alongside a significant increase in incidence and mortality in recent years. We present the case of an exceptional response to immunotherapy in a heavily pre-treated pancreatic adenocarcinoma. The patient is a 73-year-old man that was diagnosed in 2017 with locally advanced pancreatic adenocarcinoma. He underwent different lines of chemotherapy and after exhausting standard treatment options, he practiced the FoundationOne® CDx analysis (Foundation Medicine, Inc., Cambridge, MA, USA), that pointed out a High Tumor mutational burden that permitted our Oncology Center to request Pembrolizumab 200mg flat dose q 21 as an off-label therapy. The patient started the treatment in July 2021 and is still ongoing, having achieved a complete radiological response of hepatic metastases. Although immunotherapy is not part of the standard treatment paradigm for advanced pancreatic cancer, our case suggests that it may provide substantial and durable clinical benefit in a small molecularly selected subgroup of patients who have exhausted conventional therapeutic options, highlighting the critical role of comprehensive molecular profiling in identifying actionable treatment opportunities.

PubMedThe Lancet. Oncology2026-07-14

Switching to camizestrant at ESR1 mutation emergence before disease progression during first-line treatment of hormone receptor-positive advanced breast cancer (SERENA-6): extended analysis of a double-blind, placebo-controlled, randomised, phase 3 trial.

Turner Nicholas C NC, Mayer Erica L EL, Park Yeon Hee YH, Janni Wolfgang W et al.

SERENA-6 is, to our knowledge, the first global registrational study to use prospective circulating tumour DNA (ctDNA) monitoring to identify the emergence of an acquired resistance mutation before clinical progression and then direct a change in therapy in patients with hormone receptor-positive advanced breast cancer. Switching to camizestrant from aromatase inhibitor with continued cyclin-dependent kinase (CDK) 4/6 inhibitor at ESR1 mutation emergence during first-line therapy significantly improved progression-free survival at interim analysis. We report comprehensive results from ESR1 mutation surveillance in SERENA-6, updated progression-free survival, final analysis of second progression-free survival with longer follow-up, and an exploratory analysis of ESR1 mutation ctDNA dynamics on treatment to give a comprehensive report of this new treatment strategy. This double-blind, placebo-controlled, randomised, phase 3 trial was conducted at 264 hospitals and cancer centres in 23 countries and enrolled women with any menopausal status, or men, aged 18 years or older who were receiving first-line treatment with aromatase inhibitor plus CDK4/6 inhibitor for at least 6 months for oestrogen receptor-positive, HER2-negative locally advanced or metastatic breast cancer. Patients were required to have an Eastern Cooperative Oncology Group performance status score of 0 or 1. Eligible patients were enrolled and had ctDNA tested for ESR1 mutation every 2-3 months, coinciding with routine clinical assessments, using the Guardant360 CDx assay. Patients with an ESR1 mutation in ctDNA and without radiological progression were randomly assigned (1:1) using block randomisation (stratified by disease site, time of ESR1 mutation detection, time from initiation of aromatase inhibitor plus CDK4/6 inhibitor to randomisation, and CDK4/6 inhibitor) to switch to camizestrant (75 mg orally once daily) with continued CDK4/6 inhibitor (orally at the same dose) or to continue receiving aromatase inhibitor (anastrozole 1 mg or letrozole 2·5 mg orally once daily) plus CDK4/6 inhibitor (orally at the same dose as was received during ESR1 mutation surveillance phase). Palbociclib and ribociclib were dosed, orally, once daily for 21 days and then 7 days with no treatment in 28-day cycles, while abemaciclib was dosed, orally, twice daily every day in 28-day cycles. The SERENA-6 sample size was determined to ensure sufficient power for both the primary endpoint (investigator-assessed according to RECIST 1.1 progression-free survival) and the key secondary endpoint of investigator-assessed second progression-free survival (time from randomisation to disease progression after first subsequent therapy or death). For patients who had experienced a first progression, scans to assess second progression-free survival were conducted every 8-12 weeks. Updated progression-free survival analysis at this data cutoff was descriptive. Efficacy analyses included all randomly assigned patients (intention to treat). This study is registered with ClinicalTrials.gov, NCT04964934, and is ongoing. From June 30, 2021, to June 14, 2024, 3325 patients were screened and 3256 patients received at least one ESR1 mutation test during first-line therapy and 548 patients had a positive ESR1 mutation test by the time of screening closure. 315 patients (312 [99%] female; 199 [63%] White, 73 [23%] Asian, six [2%] Black or African American, 37 [12%] other, not reported, or with missing race data) were randomly assigned: 157 to camizestrant plus CDK4/6 inhibitor and 158 to aromatase inhibitor plus CDK4/6 inhibitor. After a median follow-up of 23·5 months (IQR 17·9-32·1; data cutoff Jan 2, 2026), median progression-free survival was 16·8 months (95% CI 14·7-19·4) with camizestrant plus CDK4/6 inhibitor versus 9·2 months (7·2-9·7) with aromatase inhibitor plus CDK4/6 inhibitor (hazard ratio [HR] 0·45 [95% CI 0·34-0·59]; nominal p<0·0001); consistent with previous interim analysis. Median second progression-free survival was 25·7 months (95% CI 20·4-30·3) with camizestrant plus CDK4/6 inhibitor versus 19·1 months (16·8-21·0) with aromatase inhibitor plus CDK4/6 inhibitor; HR 0·63 (0·46-0·86; p=0·0037). The most common grade 3-4 adverse events were neutropenia (42 [27%] patients in the camizestrant plus CDK4/6 inhibitor group vs 27 [17%] patients in the aromatase inhibitor plus CDK4/6 inhibitor group) and neutrophil count decreased (35 [23%] vs 30 [19%] patients), while serious adverse events were reported in 24 (15%) versus 29 (19%) patients. There were three deaths considered by the trial investigator to be possibly related to treatment (camizestrant plus CDK4/6 inhibitor group: sudden death, possibly related to camizestrant; aromatase inhibitor plus CDK4/6 inhibitor group: sepsis, possibly related to abemaciclib, and ileus, possibly related to letrozole). Switching to camizestrant plus CDK4/6 inhibitor at ESR1 mutation emergence, versus continuing aromatase inhibitor plus CDK4/6 inhibitor, resulted in sustained progression-free survival benefit that translated into a statistically significant improvement in second progression-free survival. These results further support switching endocrine treatment to camizestrant from aromatase inhibitor upon detection of ESR1 mutation, with continuation of any of the globally approved CDK4/6 inhibitor, to extend first-line treatment benefit. AstraZeneca.

PubMedFrontiers in oncology2026-07-13

A case report of primary mucinous adenocarcinoma of the bladder and literature review.

Li Yue Y, Peng Xuefeng X, Jin Suiyang S, Wang Qiang Q

Primary mucinous adenocarcinoma of the bladder is a rare and highly aggressive malignancy. Its diagnosis is challenging due to the need to exclude metastatic gastrointestinal adenocarcinoma, and standardized treatment protocols are lacking. Here, we report a case of primary bladder mucinous adenocarcinoma in a 70-year-old female who presented with urinary difficulty without hematuria. The diagnostic workup integrated endoscopic evaluation with immunohistochemical markers (CK7-, CK20+, CDX-2+, β-catenin membrane+, SATB2-, GATA3-) to rule out a colorectal primary. The patient underwent transurethral resection followed by robot-assisted radical cystectomy (pT4aN0M0) but declined adjuvant therapy for personal reasons. At 6-month follow-up, no recurrence or metastasis was detected. This case highlights the diagnostic utility of a targeted immunohistochemical panel, the real-world complexity of treatment decisions in the absence of guidelines, and is compared with all reported cases from the past decade in a structured literature review.

PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-07-12

Shiyiwei Shenqi Pian-derived quercetin reactivates apoptosis in clear cell renal cell carcinoma by destabilizing survivin and x-linked inhibitor of apoptosis protein.

Zhang Dong D, Li Shenglong S, Zhang Xi X, Guo Qian Q et al.

Clear cell renal cell carcinoma (ccRCC) strongly resists apoptosis via baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) and X-linked inhibitor of apoptosis protein (XIAP). Meanwhile, the specific anti-ccRCC mechanisms of the pro-apoptotic herbal mixture Shiyiwei Shenqi Pian (SSP) remain undefined. To systematically discover the key bioactive compound within SSP and characterize its precise mechanism of action in uncoupling the oncogenic BIRC5-XIAP complex. An advanced integrative strategy combining network pharmacology, transcriptomic profiling, machine-learning, and structural dynamic simulations was utilized to screen and predict therapeutic targets. The in silico findings were then rigorously and sequentially validated across multiple experimental platforms, progressing from in vitro cell models to in vivo CDX and PDX settings. A multi-omics framework was applied to investigate the mechanisms of SSP in ccRCC. Active compounds and disease-related targets were identified through database mining and UPLC-Q-TOF-MS profiling, followed by machine-learning-based prioritization. Molecular interactions were analyzed using docking, molecular dynamics simulations, and single-cell transcriptomics. Protein interactions and stability were validated by co-immunoprecipitation (Co-IP), microscale thermophoresis (MST), cycloheximide (CHX)-chase, and ubiquitination assays. Cellular effects were assessed by proliferation and apoptosis assays, while in vivo efficacy was evaluated using CDX and PDX models. Shared SSP-ccRCC targets were enriched in apoptosis-related pathways, and intact SSP extract suppressed ccRCC cell proliferation and clonogenic growth in vitro. Multi-cohort machine-learning modeling identified BIRC5 as a key prognostic target. Among the major SSP-derived compounds, quercetin showed favorable binding to BIRC5 and XIAP and was selected for mechanistic validation. Single-cell and bulk transcriptomic analyses confirmed co-enrichment and positive correlation of BIRC5 and XIAP in ccRCC. Mechanistically, quercetin disrupted the BIRC5-XIAP complex, weakened their direct protein interaction, and accelerated ubiquitin-mediated degradation of both proteins. This process restored caspase activation and induced caspase-dependent apoptosis, leading to reduced cell proliferation and colony formation. In CDX and PDX models, quercetin suppressed tumor growth and reduced BIRC5/XIAP pathway activity. Quercetin was identified as a major mechanistically validated active constituent of SSP. It suppresses ccRCC growth by destabilizing the BIRC5-XIAP anti-apoptotic complex and reactivating caspase-dependent apoptosis, supporting its potential as a therapeutic lead for ccRCC.

PubMedNPJ genomic medicine2026-07-12

Specimen quality shapes the actionable genomic landscape in comprehensive cancer genomic profiling.

Nakahara Hikaru H, Niitsu Hiroaki H, Motonaga Masanori M, Matsuo Hiroaki H et al.

Comprehensive genomic profiling (CGP) is widely used to identify actionable alterations and guide precision oncology, yet only a minority of tested patients receive genome-matched therapies, underscoring a gap between genomic findings and clinical benefit. We hypothesized that this gap may partly reflect variation in the reliability and interpretability of genomic information generated from specimens of different quality and by different assay modalities. To examine this possibility, we performed a retrospective multicenter analysis of 2002 CGP tests conducted between 2019 and 2025 across 13 institutions in Japan. Detection of short variants, copy number alterations (CNAs), structural variants, and genomic signatures, including microsatellite instability, tumor mutational burden, and homologous recombination deficiency signature, was compared among FoundationOne CDx specimens classified as pass (F1-pass) or qualified (F1-qual) and liquid-based CGP (liq-CGP). Short variant detection remained largely preserved in F1-qual specimens, whereas CNA and genomic signature detection were substantially reduced. In pancreatic adenocarcinoma, KRAS variants were detected in 93% of F1-pass, 88% of F1-qual, and 57% of liq-CGP cases. These differences affected the proportion of patients offered genome-matched therapies. Machine learning models predicted QC status with area-under-the-curve values of 0.72-0.78. Our findings support QC-aware CGP selection in routine precision oncology.

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