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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

PubMedFrontiers in oncology2026-09-18

Case Report: Radical nephroureterectomy after toripalimab plus disitamab vedotin in biomarker-non-enriched upper tract urothelial carcinoma.

Cheng Guohui G, Zhang Quan Q, Li Rundong R, Zhou Zhongze Z et al.

Upper tract urothelial carcinoma (UTUC) is uncommon and aggressive, and evidence for perioperative antibody-drug conjugate or immunotherapy remains limited. We report a 59-year-old man with biomarker-non-enriched high-risk ureteral UTUC treated with four cycles of toripalimab plus disitamab vedotin before planned surgery. Magnetic resonance urography, urine cytology, and ureteroscopic biopsy supported high-grade UTUC with glandular differentiation; CDX-2, villin, and β-catenin positivity prompted exclusion of a gastrointestinal primary. The biopsy showed HER2 0, TROP2 0, and low PD-L1 expression. Restaging MRI and endoscopy demonstrated reduced visible lesion extent; axial dimensions decreased from 3.68 × 2.69 cm to 2.14 × 1.55 cm. No formal RECIST 1.1 category was assigned because imaging was not standardized. The patient then underwent planned laparoscopic radical nephroureterectomy with bladder cuff excision. Final pathology showed poorly differentiated ureteral urothelial carcinoma with marked histological heterogeneity, staged ypT2Nx. Recovery was uneventful. At the latest follow-up on May 28, 2026, the patient remained well, and surveillance cystoscopy showed no evident intravesical abnormality. This case highlights the limited representativeness of pretreatment biopsy in UTUC. The observed lesion reduction is hypothesis-generating and should not be interpreted as evidence of clinical efficacy. Standardized response assessment and longer follow-up are required.

PMID 42755500
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PubMedOncogene2026-09-16

CircLAMA5 traps Sam68 in the cytoplasm to regulate alternative splicing and drive sunitinib resistance in ccRCC.

Xu Zhehao Z, Lu Haohua H, Lu Zeyi Z, Wang Ruyue R et al.

Tyrosine kinase inhibitor (TKI) resistance remains a major challenge in the treatment of clear cell renal cell carcinoma (ccRCC), yet the underlying molecular mechanisms are not fully understood. Here, we identify circular RNA circLAMA5 (hsa_circ_0061093) as a critical driver of sunitinib resistance in ccRCC. CircLAMA5 is significantly upregulated in sunitinib‑resistant cell lines and cell‑derived xenografts (CDX-R). Functional studies demonstrate that circLAMA5 enhances ccRCC cell survival, colony formation, and apoptosis evasion under sunitinib treatment both in vitro and in vivo. Mechanistically, circLAMA5 binds to the C-terminal region of Sam68 and promotes its cytoplasmic retention, at least in part by impairing the interaction between Sam68 and the nuclear import receptor TNPO1. This reduces nuclear Sam68 availability and suppresses its regulatory role in the alternative splicing of Bcl-x pre-mRNA, leading to a decreased pro‑apoptotic Bcl‑x(s)/anti‑apoptotic Bcl‑x(L) ratio and ultimately conferring sunitinib resistance. Importantly, we developed a biomimetic nanoparticle system coated with ccRCC cell membranes (RCCM@NPs) for targeted delivery of sh‑circLAMA5, effectively restoring sunitinib sensitivity in resistant tumors in vivo. Our findings reveal circLAMA5 as a key regulator of sunitinib resistance via the Sam68‑Bcl‑x splicing axis and propose a promising targeted nanotherapeutic strategy for overcoming resistance in advanced ccRCC.

PMID 42744974
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PubMedSurgical case reports2026-09-11

Medullary Carcinoma of the Ascending Colon in an Older Woman: A Case Report.

Kishimoto Ayana A, Yamamoto Tetsu T, Taniura Takahito T, Ishitobi Kazunari K et al.

Medullary carcinoma of the colon is a rare histological subtype of poorly differentiated or undifferentiated adenocarcinoma, with a reported incidence of 0.05%-0.08%. It typically affects older women, is more frequently located in the right colon, and is characterized by a high prevalence of mismatch repair deficiency, particularly microsatellite instability (MSI). In comparison to other poorly differentiated adenocarcinomas, medullary carcinoma generally exhibits a lower rate of lymph node or distant metastasis and carries a relatively favorable prognosis. Due to its recent classification and rarity, reported cases remain limited. We herein describe a case of surgically resected medullary carcinoma of the ascending colon in an older woman, along with a brief review of the relevant literature. An 88-year-old woman presented with unintentional weight loss of 4 kg over 3 months. Colonoscopy revealed a type 2 tumor in the ascending colon, and biopsy demonstrated poorly differentiated adenocarcinoma. Imaging showed asymmetric wall thickening without lymph node or distant metastasis, and the clinical diagnosis was ascending colon cancer, cT3N0M0, Stage IIA. She underwent an elective laparoscopic right hemicolectomy with D3 lymphadenectomy. The postoperative course was uneventful. A histopathological examination showed sheets of atypical cells with enlarged nucleoli, expansive growth, a Crohn's-like lymphoid reaction, and focal signet-ring-like features. Immunohistochemistry demonstrated positivity for MUC5AC, partial positivity for MUC2, focal positivity for CK20 and CDX-2, retained expression of MSH2 and MSH6, and loss of MLH1 and PMS2 expression, indicating deficient mismatch repair (dMMR), which supports the diagnosis of medullary carcinoma. The final pathological staging was pT3N0M0, Stage IIA. Given the absence of lymph node metastasis and the patient's advanced age, adjuvant chemotherapy was not administered. She has remained recurrence-free for 4 years under active surveillance. Colonic medullary carcinoma is a rare tumor that predominantly occurs in older patients and generally demonstrates a more favorable prognosis than other poorly differentiated adenocarcinomas. Treatment decisions should be based primarily on tumor stage. Although preoperative diagnosis is often difficult, awareness of its characteristic features may help avoid excessive therapeutic de-escalation.

PMID 42725321
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PubMedAnnals of translational medicine2026-09-10

Individualized pharmacotherapy: background and development.

Jørgensen Jan Trøst JT, Westergaard Niels N

Most drug prescriptions are still based on empiricism and not on solid biological data, which often results in considerable patient variability and, sometimes, low patient benefits. Although variability in patient response to pharmacotherapy has long been recognized, only in recent decades have new molecule analytical methods provided insight into some of the causes, which are often related to somatic or germline genetic variations. Based on this insight, different predictive biomarker tests have been developed to optimize and individualize pharmacotherapy. These biomarker tests are classified as companion diagnostic (CDx) or pharmacogenetic (PGx) tests. In both the United States and Europe, CDx and PGx information is part of the regulatory drug labeling and is included in the Prescribing Information for the individual drugs and biologics. In the United States, this type of information is found in the labeling of more than 400 regulatory-approved drugs and biological products. Despite these measures and the documented clinical utility of CDx and PGx testing, clinical implementation is lagging, especially with regard to PGx. There are various reasons for the lack of testing, such as insufficient education and awareness among healthcare professionals, inadequate access to biomarker testing, regulatory hurdles, and insufficient reimbursements. Although progress has been made in recent years, further efforts are needed to fully realize the potential of individualized pharmacotherapy by integrating the use of predictive biomarkers into routine clinical practice.

PMID 42718847
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PubMedBiochimica et biophysica acta. Molecular basis of disease2026-09-10

CAPN1 promotes the progression of MLL-rearranged acute myeloid leukemia by suppressing SHP-1 and activating MAPK/ERK signaling pathway.

Liu Jia-Yin JY, Cao Xu X, Lu Yan-Ling YL, Hu Man-Man MM et al.

The MLL-rearranged (MLL-r) acute myeloid leukemia (AML) represents a hematological malignancy with a dismal prognosis and a pressing demand for innovative therapeutic targets. CAPN1 is overexpressed in MLL-r AML and predicts poor prognosis, however, its roles in MLL-r AML remains unclear. Prognostic value of CAPN-1 was evaluated using logistic regression and receiver operating characteristic (ROC) analyses. Roles of CAPN-1 were assessed in MOLM13, MV4-11 and NOMO-1 cells with CAPN-1 knockdown or overexpressed using CCK-8, colony formation, flow cytometry, and CDX mouse models. Mechanistic studies were conducted via RNA sequencing, co-IP, IF and molecular docking, focusing on the CAPN1-SHP-1-MAPK/ERK signaling axis. The expression of CAPN1 was the highest in the MLL-r subtype among different AML subtypes, correlating with adverse clinical outcomes. CAPN1 knockdown markedly suppressed proliferation and clonogenic capacity, induced apoptosis, and caused G2/M arrest, whereas CAPN1 overexpression displayed opposite results, and this pro-leukemic functions were dependent on its proteolytic activity. In vivo, CAPN1 knockdown prolonged survival and reduced leukemic infiltration of mouse in xenograft models, while its overexpression accelerated disease progression. Mechanistically, CAPN1 directly interacted with SHP-1 and reduced its stability via protease function, thereby enhancing MAPK/ERK phosphorylation. Pharmacological reactivation of ERK signaling by ceramide C6 treatment rescued the apoptosis and G2/M arrest induced by CAPN1 knockdown. CAPN1 acts as a novel prognostic biomarker and oncogenic driver in MLL-r AML by interacting with and suppressing SHP-1 to activate the MAPK/ERK pathway, highlighting the CAPN1-SHP-1-MAPK/ERK axis as a promising therapeutic target in the MLL-r AML subtype.

PMID 42722135
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-09-09

Discovery and Optimization of AMT-676, a CDH17-Targeting ADC for the Treatment of Advanced Gastrointestinal Cancers.

Wang Ying-Nan YN, Ruan Dan-Yun DY, Shi Jing J, Huang Yue Y et al.

Advanced-stage gastrointestinal (GI) cancers present an unmet need for innovative therapies, and antibody-drug conjugates (ADCs) offer promising solutions. This study investigates the antitumor efficacy and toxicity of AMT-676, a novel ADC targeting Cadherin 17 (CDH17), in GI cancers. Utilizing MabArray screening and immunohistochemistry, CDH17 was identified as a promising ADC target in GI tumors with minimal expression in healthy organs. The ADC was optimized through comprehensive in vitro and in vivo evaluations of binding affinity, cytotoxicity, pharmacokinetics, and toxicity, with antitumor potential evaluated using cell line-derived (CDX) and patient-derived tumor xenograft (PDX) models. Leveraging the T moiety-exatecan platform, we synthesized AMT-676, comprising a high-affinity CDH17-specific antibody, a hydrophilic self-immolative T1000 linker, and exatecan with a Drug-to-Antibody Ratio (DAR) of 4. AMT-676 demonstrated sustained antitumor responses across CDX and PDX GI models with diverse CDH17 expression, notably inhibiting metastatic growth in a colorectal cancer model. Cynomolgus monkey studies revealed favorable pharmacokinetics and manageable toxicity associated with AMT-676. In conclusion, we developed a novel CDH17-targeting ADC characterized by a high therapeutic index and tolerable toxicity profile, highlighting its promise for GI cancer treatment. A first-in-human, phase I clinical trial of AMT-676 in patients with advanced solid tumors is currently underway (NCT06400485).

PMID 42713665
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