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TLX007-CDx (TLX007 CDx / TLX007CDx)

✓ Approved

Telix Pharmaceuticals Limited · 影像药物 · 影像药物

什么是 TLX007-CDx？

TLX007-CDx 是一种影像药物，由Telix Pharmaceuticals Limited研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名TLX007 CDx, TLX007CDx
公司Telix Pharmaceuticals Limited
药物类别影像药物
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, Telix Pharmaceuticals Limited

治疗适应症

TLX007-CDx 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Prostate cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancerBLA/NDA

相关研究文献

PubMedOncogene2026-08-04

Bispecific ANXA2/CD147 CAR-T cell therapy for osteosarcoma.

Tang Hai-Jun HJ, Dai Wei W, Xiao Dan-Ting DT, Li He-Ning HN et al.

Osteosarcoma is a highly malignant tumor with poor prognosis. Current CAR-T cell therapies for osteosarcoma are predominantly designed with single targets, but their efficacy remains unsatisfactory. In this study, a novel bispecific CAR-T cell was developed to provide an experimental basis for improving the therapeutic outcome of osteosarcoma. Single-cell RNA sequencing (scRNA-seq) identified two antigens highly expressed in osteosarcoma cells, ANXA2 and CD147, whose expression was further validated at the tissue level by qRT-PCR, flow cytometry, and immunohistochemistry. Based on a second-generation CAR backbone, a bispecific ANXA2/CD147 CAR-T construct was generated using magnetic bead sorting, primary T-cell culture, and lentiviral transduction, achieving a transduction efficiency of 47.1%. LDH release assays demonstrated that bispecific CAR-T cells exhibited significantly greater cytotoxicity against tumor cells than single-target and control groups. ELISA confirmed that bispecific CAR-T cells released higher levels of effector molecules, including GZMB and TNFα. In a subcutaneous CDX model, bispecific CAR-T cells displayed superior antitumor activity and greater T-cell infiltration. In a paw pad xenograft model, mice treated with bispecific CAR-T cells exhibited the smallest tumor volumes, lowest tumor weights, and reduced rates of lymph node metastasis. Furthermore, PDX models confirmed that bispecific CAR-T cells effectively suppressed osteosarcoma growth. ScRNA-seq of tumors derived from CDX models and immunohistochemistry revealed markedly increased infiltration of M1 macrophages in the bispecific group. Collectively, this study successfully generated a bispecific ANXA2/CD147 CAR-T cell with robust antitumor activity, providing a promising new strategy for the immunotherapy of osteosarcoma.

PMID 42547556
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PubMedJournal of ultrasound2026-08-02

Serial scrotal ultrasonographic evolution of testicular metastasis from gastric adenocarcinoma: a case description.

Huang Libing L, Li Xiao X, Fang Zhenyan Z, Wen Zonghua Z et al.

Testicular metastasis from gastric adenocarcinoma is rare, and serial ultrasonographic evolution of this process has seldom been documented. We report a 79-year-old man with gastric adenocarcinoma who presented with progressive left-dominant scrotal enlargement. Initial scrotal ultrasonography showed bilateral hydroceles, greater on the left, with septation but no definite intratesticular lesion. One month later, repeat ultrasonography demonstrated heterogeneous left testicular echotexture with multiple small solid nodules and mildly increased vascularity, indicating interval parenchymal involvement. Pelvic magnetic resonance imaging showed bilateral suspicious testicular and epididymal abnormalities with septal enhancement and diffusion restriction. Histopathology confirmed metastatic adenocarcinoma involving the left testis and left tunica vaginalis, with CDX-2 and SATB2 positivity supporting gastrointestinal differentiation. Biopsy of the right tunica vaginalis showed hydrocele without evidence of malignancy; therefore, the contralateral abnormalities remained radiologically suspicious but were not pathologically confirmed. Follow-up ultrasonography demonstrated destructive progression of the left testis and epididymis with chaotic vascularity. This case highlights the value of serial scrotal ultrasonography for recognizing interval progression from apparently benign hydrocele-dominant findings to metastatic testicular-epididymal involvement. In older patients with known extratesticular malignancy, evolving scrotal swelling should prompt careful reassessment of testicular parenchyma and vascularity on follow-up ultrasound.

PMID 42541655
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PubMedJournal of the anus, rectum and colon2026-08-02

Single-center Experience with Comprehensive Genomic Profiling Using Circulating Tumor DNA for Metastatic Colorectal Cancer.

Ito Kazuma K, Kataoka Kozo K, Muroi Yoshiko Y, Koba Mizuki M et al.

Comprehensive genomic profiling (CGP) using circulating tumor DNA (ctDNA) has recently become available in Japan, but its clinical utility in daily practice remains unclear. We retrospectively evaluated 19 patients with metastatic colorectal cancer (mCRC) who underwent plasma-based CGP (Guardant360 CDx) between November 2023 and May 2025. ctDNA was detected in 18 of 19 patients (95%) with previously treated mCRC. The median turnaround time from blood collection to result was 11 days (range: 7-15). The median number of gene alterations was 5 (range: 1-29), and pathogenic/likely pathogenic alterations were identified in 15 patients (79%). ctDNA was preferentially selected over tissue CGP in patients with small tumor burden, lack of contemporary tumor sample, or double cancer (considering spatial and temporal heterogeneity). Three patients initially identified with RAS mutant tumors by tissue were subsequently identified as RAS wild-type by plasma CGP. Those were treated with anti-epidermal growth factor receptor (EGFR) therapy, resulting in partial response or stable disease. These observations suggest that plasma-based CGP may provide additional molecular information that could be clinically informative in mCRC in a real-world setting. Although the findings should be interpreted as exploratory, re-evaluation of molecular profiles using ctDNA enabled the exploratory identification of NeoRAS wild-type patients, who could potentially benefit from anti-EGFR therapy.

PMID 42539883
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PubMedJournal of animal science and biotechnology2026-08-02

Age- and sex-related differences in early-life gut microbiota and intestinal physiology in broiler chickens.

Corion Matthias M, Akram Muhammad Zeeshan MZ, Arévalo Sureda Ester E, Comer Luke L et al.

Early-life sex identification technologies are making sex-specific management increasingly feasible in broiler production, yet limited information exists on how males and females differ in the development of their gut ecosystem. While sex-related variation in growth rate and endocrine physiology is well established, much less is known about potential differences in gut morphology, barrier function, microbiota assembly, and intestinal gene expression during the starter period, where early performance divergence between males and females begins to emerge. A clearer understanding of these early-life processes is essential to refine sex-specific nutrition and management strategies. Therefore, this study investigated sex-related differences in gut morphology, intestinal permeability, microbiota composition and predicted functionality, as well as ileal gene expression related to nutrient transport, barrier function, immune response, and metabolic signaling in broilers at 7, 14, and 21 days of age. Body weight followed a typical early-life pattern and differed between sexes only at d 21, when males were heavier. Gut morphology matured similarly in both sexes, whereas gut permeability declined with age and was lower in males at d 20, suggesting a slightly tighter intestinal barrier. Microbiota structure was predominantly shaped by age, but sex-related divergence emerged with maturation from d 14 onward, especially in the cecum: males were enriched in strict anaerobic fermenters and carbohydrate-degradation/short-chain fatty acid (SCFA)-related pathways, while females showed higher abundance of Romboutsia, Flavonifractor, and other taxa linked to proteolytic metabolism and the degradation of aromatic amino acid-derived compounds. Gene expression was mainly driven by age, yet consistent sex-specific transcriptional signatures were revealed. Males were more associated with nutrient transport (e.g., SLC15A1, SLC30A1, SLC5A1) and epithelial functional maturation profiles (e.g., CDX) over time, whereas females were more associated with tight-junction integrity (e.g., OCLN) and amino-acid sensing/transport markers (e.g., T1R1, SLC3A1). Cecal SCFA concentrations were measured at d 21, yet no differences were found. Overall, gut development was largely age-driven, but sex-specific differences in barrier function, microbiota composition and function, and epithelial gene expression emerged with maturation, without differences in gut morphology or luminal SCFA concentrations.

PMID 42542545
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PubMedbioRxiv : the preprint server for biology2026-08-01

Ribonucleotide Reductase Inhibition Overcomes FLT3 Inhibitor Resistance in Acute Myeloid Leukemia.

Tian Zhen Z, Wei Xiaoyu X, Chatla Srinivas S, Liu Yang Y et al.

Internal tandem duplication mutations in FLT3 ( FLT3 ITD ) occur in approximately 30% of patients with acute myeloid leukemia (AML) and are among the most common genetic alterations in this disease. FLT3 ITD is a major driver of AML and is associated with poor clinical outcomes. Although FLT3 inhibitors (FLT3is) have significantly improved outcomes for patients with FLT3 ITD + AML, acquired resistance remains a major barrier to durable clinical benefit. Reactivation of RAS/MAPK signaling, often driven by activating NRAS mutations, is a major mechanism of FLT3i resistance in AML; however, effective strategies to overcome this resistance remain lacking. Here, we identify ribonucleotide reductase (RNR) as a critical therapeutic vulnerability in NRAS -driven FLT3i-resistant FLT3 ITD + AML. Activation of RAS signaling through SPRY3 loss or oncogenic NRAS mutations confers robust resistance to FLT3is, whereas pharmacologic inhibition of RNR with multiple inhibitors, as well as siRNA-mediated RNR suppression, reverses FLT3i resistance and restores FLT3i sensitivity across multiple FLT3 ITD + AML models in vitro . In vivo , clofarabine, an FDA-approved RNR inhibitor (RNRi), significantly overcomes NRAS mutation-driven FLT3i resistance. In combination with FLT3 inhibition, clofarabine markedly suppresses the progression of FLT3i-resistant AML and significantly prolongs survival in cell line-derived xenograft (CDX) models. Importantly, the therapeutic efficacy of the gilteritinib/clofarabine combination was independently validated in two genetically distinct patient-derived xenograft (PDX) models harboring different NRAS mutations, demonstrating robust reduction of leukemia burden and confirming the generalizability of RNR inhibition in primary FLT3i-resistant AML. Together, these findings identify a previously unrecognized therapeutic vulnerability in FLT3i-resistant FLT3 mut + AML and establish RNR inhibition as an effective strategy to overcome FLT3i resistance, providing a strong rationale for the clinical evaluation of RNRis in combination with FLT3is in patients with resistant AML. Although FLT3 inhibitors (FLT3i) are an important therapeutic advance in FLT3 ITD + AML, resistance commonly develops. We identified ribonucleotide reductase (RNR) as a new key vulnerability in NRAS -driven FLT3i-resistant AML and demonstrated that multiple RNRis, including the FDA-approved agent clofarabine, restore FLT3i sensitivity and enhance antileukemic activity, supporting a clinically actionable combination strategy.

PMID 42539318
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PubMedLaboratory investigation; a journal of technical methods and pathology2026-07-31

Real World Evaluation of AI-Based Tumor Cell Content Quantification for Molecular Tumor Profiling.

Gachechiladze Mariam M, Runge Jan-Niklas JN, Kull Tobias T, Schnoz Christina C et al.

Repeated evidence demonstrates limited reproducibility and accuracy of the visual quantification (VQ) of the tumor cell content (TCC) by clinical pathologists for downstream molecular testing. Artificial intelligence (AI)-based digital quantification (DQ) of TCC represents a promising alternative, yet real-world evidence from routine molecular diagnostic workflows remain limited. In this study, we evaluated the analytical performance and practical aspects of analytical validation process of an AI-based DQ tool in routine molecular diagnostics. The clinical-grade AIM-TumorCellularity (AIM-TC; PathAI©) workflow was tested in molecular diagnostics for samples analyzed by comprehensive genomic profiling (FoundationOne®CDx (F1CDx), Foundation medicine Inc.). The cohort included 300 non-paired resection, biopsy, and cytology/cell block) specimens from primary and metastatic breast (n = 66), lung (n = 117), colorectal (n = 40), pancreatic (n = 38), and prostate (n = 39) cancers, reflecting real-world diagnostic sample heterogeneity of a tertiary care center. We compared TCC estimates generated by pathologists' VQ, AI-based DQ, and molecular quantification (MQ) by bioinformatic deconvolution. Agreement was lowest between VQ and MQ (Spearman Rs = 0.38) and between VQ and DQ (Rs = 0.44), while DQ showed stronger concordance with MQ (Rs = 0.63). Single-cell validation against expert ground truth demonstrated high performance of DQ in tumor cell detection, with sensitivity of 0.98.5, specificity of 0.99, and accuracy of 0.99, based on 27,958 annotated cells across 60 regions of interest comparable to microscopic high-power fields. Analysis of pre-analytical and analytical factors identified specimen type and cautery/crush artifacts as the main pre-analytical contributors to DQ-VQ discrepancies, while overall variations in specimen cellularity was the dominant analytical factor. In summary, this study provides the first comprehensive real-world evaluation of AI-based TCC quantification in routine molecular pathology workflow, highlighting its robustness, accuracy, and the critical role of pre-analytical standardization, as well as pathologists` oversight for successful clinical implementation.

PMID 42532480
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