Osimertinib Plus Capivasertib in NSCLC With PIK3CA/AKT1/PTEN Alterations Following Prior 1L Osimertinib

NCT07486648 | Not Yet Recruiting Phase 1 DMC

• 1 other identifier: ESR-25-22924
• Study Type: interventional
• Target: 53
• Locations: 1 country
• Sites: 2

Brief Summary

The goal of this clinical trial is to learn if Osimertinib plus Capivasertib works to treat EGFRm advanced non-small cell lung cancer (NSCLC) in participants with PIK3CA/AKT1/PTEN alterations after progression on first-line Osimertinib (monotherapy or plus chemotherapy). The main questions it aims to answer are: Part A:

• Number of Dose-limiting toxicities (DLTs)
• Adverse events (AEs)/serious adverse events (SAEs) (graded by CTCAE Version 5.0)
• Recommended combined dose (RCD) Part B:Confirmed ORR assessed by the Investigator per RECIST 1.1 criteria. Participants will: Part A:Take Capivasertib twice daily from day 1 to 4 of a 7-day cycle, Osimertinib will be given orally QD(once daily) at 80 mg throughout the study treatment period. Part B: Take Osimertinib (80mg QD, continuously) and Capivasertib(RCD,orally BID from day1-day 4 in 7-day cycle , 4 days on /3 days off) till disease progression (PD) or unacceptable toxicity.

Conditions

Lung Cancer (NSCLC); Lung Cancer (Non-Small Cell); Advanced Non-small-cell Lung Cancer

Keywords

NSCLC; Osimertinib plus Capivasertib

Outcome Measures

Primary Outcomes (4)

• Part A Number of Dose-limiting toxicities (DLTs)

  A DLT is defined as any toxicity related to study drug and not attributable to the disease or disease-related processes under investigation, which occurs from the first dose of study treatment (Day 1, Cycle 0) up to the last day of Cycle 1 (28 days after start of dosing)

  28 days post first dose of study treatment

• Part A Adverse events (AEs)/serious adverse events (SAEs) (graded by CTCAE Version 5.0)

  From the time of signature of informed consent form up to 44 months

• Part A Recommended combined dose (RCD)

  The RCD is defined as the optimal dose combination of study drugs, established based on integrated assessment of safety and relevant available data from dose escalation phase

  From first dose of study treatment up to 12 months

• Part B Confirmed ORR assessed by the Investigator per RECIST 1.1 criteria

  ORR is defined as the percentage of participants who have at least one confirmed response of CR or PR prior to any evidence of progression (as determined by investigator at local site per RECIST 1.1)

  5 months post first dose of study treatment

Secondary Outcomes (8)

• Part A Confirmed ORR assessed by the Investigator per RECIST 1.1 criteria

  5 months post first dose of study treatment

• Part B Progression-free survival(PFS)

  From first dose of study treatment up to 27 months

• Part B Duration of response(DoR )

  From 1 months post first dose of study treatment up to 27 months

• Part B Disease control rate(DCR)

  From 2 months post first dose of study treatment up to 27 months

• Part B Overall survival(OS)

  From first dose of study treatment up to 27 months

Study Arms (1)

Capivasertib 320/400 mg in combination with Osimertinib 80mg

EXPERIMENTAL

Capivasertib 320/400 mg (twice daily from day 1 to 4 of a 7-day cycle ),Osimertinib 80 mg( once daily continuously),28 days per cycle

Drug: Capivasertib in combination with Osimertinib

Interventions

Capivasertib in combination with Osimertinib DRUG

Capivasertib 320/400 mg(twice daily from day 1 to 4 of a 7-day cycle ),Osimertinib 80 mg(once daily continuously),28 days per cycle

Capivasertib 320/400 mg in combination with Osimertinib 80mg

Eligibility Criteria

• Age: 18 Years+
• Sex: all
• Healthy Volunteers: No
• Age Groups: Adult (18-64), Older Adult (65+)

You may qualify if:

• Informed consent
• Provision of signed and dated, written informed consent form (ICF) prior to any mandatory and non-mandatory study-specific procedures, sampling and analyses
• Age
• Male or female age ≥18 years at the time of signing the ICF.
• Type of participant and disease characteristics
• Histologically or cytologically confirmed non-squamous locally advanced or metastatic NSCLC which is not amenable to curative therapy.
• Documented EGFR sensitive mutations (exon19 deletion, L858R mutation) prior to the first-line EGFR-TKI therapy.
• Documented radiologic progression on first-line treatment with Osimertinib monotherapy or Osimertinib plus chemotherapy:
• Participants treated with Osimertinib in the adjuvant setting can be included if progression occurred \< 6 months after last dose.
• Participants must be immunotherapy (i.e., programmed cell death protein 1 \[PD-1\] inhibitor, programmed cell death protein 1 ligand 1 \[PD-L1\] inhibitor, Cytotoxic T-lymphocyte associated protein 4 inhibitor) naïve in the metastatic setting.
• Prior immunotherapy in the neoadjuvant or adjuvant setting is acceptable providing treatment was completed more than 6 months before metastatic/recurrent disease was diagnosed.
• Mandatory provision of the required number of FFPE tumour tissue samples for PIK3CA mutations and/or AKT1 mutations and/or PTEN loss-of-function (LOF) mutations testing, which fulfils the following requirements:
• Obtained following progression on previous Osimertinib monotherapy or Osimertinib plus chemotherapy as first-line treatment.
• Specimen to meet the requirements defined in the Central Laboratory Manual and Diagnostic Testing Manual.
• Have PIK3CA and/or AKT1 and/or PTEN alterations as determined by NGS testing by a sponsor designated central laboratory on tumour specimen collected following progression on prior Osimertinib treatment.

You may not qualify if:

• Medical conditions
• Patients harbouring concurrent actionable driver mutations with locally approved targeted therapies (e.g., MET amplification) will be excluded.
• Past medical history of interstitial lung disease (ILD), drug-induced ILD, radiation pneumonitis which required steroid treatment, or any evidence of clinically active ILD.
• Clinically significant abnormalities of glucose metabolism as defined by any of the following:
• Fasting glucose ≥7.0 mmol/L (126 mg/dL) or 2 hours after glucose solution intake, blood glucose ≥11.1 mmol/L (200 mg/dL).
• HbA1c ≥8.0% (63.9 mmol/mol) at screening. Note: for any patient with evidence of impaired glucose control or insulin resistance refer to the Capivasertib Toxicity Management Guidelines.
• Any evidence of severe or uncontrolled systemic diseases, including uncontrolled hypertension and active bleeding diatheses, which in the investigator's opinion makes it undesirable for the patient to participate in the trial or which would jeopardize compliance with the protocol, or active infection (e.g. patients receiving treatment for infection) including hepatitis C and human immunodeficiency virus (HIV), or active uncontrolled hepatitis B virus (HBV) infection, or active tuberculosis infection (clinical evaluation that may include clinical history, physical examination and radiographic findings, or tuberculosis testing in line with local practice) .
• Screening for chronic conditions is not required.
• Spinal cord compression, leptomeningeal metastasis, or brain metastases unless asymptomatic, stable, and not requiring steroids for at least 4 weeks prior to start of study intervention.
• Any of the following cardiac criteria:
• Mean resting corrected QTc \>470 msec, obtained from triplicate electrocardiograms (ECGs), using the screening clinic ECG machine derived QTc value.
• History of QT prolongation associated with other medications that required discontinuation of that medication.
• Any clinically important abnormalities in rhythm, conduction or morphology of resting ECG e.g., complete left bundle branch block, third degree heart block and second-degree heart block.
• Medical history significant for arrhythmia (e.g., multifocal premature ventricular contractions, bigeminy, trigeminy, ventricular tachycardia), which is symptomatic or requires treatment (Common Terminology Criteria for Adverse Events \[CTCAE\] Grade 3), symptomatic or uncontrolled atrial fibrillation despite treatment, or asymptomatic sustained ventricular tachycardia. Participants with atrial fibrillation controlled by medication or arrhythmias controlled by pacemakers may be permitted to enter the study based on the Investigator judgement with cardiologist consultation recommended.
• Patient with any factors that increase the risk of QTc prolongation or risk of arrhythmic events such as electrolyte abnormalities including:

Sponsors & Collaborators

• Shanxi Province Cancer Hospital: lead
• Cancer Institute and Hospital, Chinese Academy of Medical Sciences: collaborator

Study Sites (2)

Cancer Hospital Chinese Academy of Medical Sciences

Beijing, Beijing Municipality, China

Location

Shanxi Cancer Hospital

Taiyuan, Shanxi, China

Location

Related Publications (36)

• Masters GA, Temin S, Azzoli CG, Giaccone G, Baker S Jr, Brahmer JR, Ellis PM, Gajra A, Rackear N, Schiller JH, Smith TJ, Strawn JR, Trent D, Johnson DH; American Society of Clinical Oncology Clinical Practice. Systemic Therapy for Stage IV Non-Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update. J Clin Oncol. 2015 Oct 20;33(30):3488-515. doi: 10.1200/JCO.2015.62.1342. Epub 2015 Aug 31.

  PMID: 26324367 BACKGROUND

• Eisenhauer EA, Therasse P, Bogaerts J, Schwartz LH, Sargent D, Ford R, Dancey J, Arbuck S, Gwyther S, Mooney M, Rubinstein L, Shankar L, Dodd L, Kaplan R, Lacombe D, Verweij J. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer. 2009 Jan;45(2):228-47. doi: 10.1016/j.ejca.2008.10.026.

  PMID: 19097774 BACKGROUND

• Chinese Society of Clinical Oncology. Non-small Cell Lung Cancer. 2025.

  BACKGROUND

• Lu S, Wu L, Jian H, Cheng Y, Wang Q, Fang J, et al. VP9-2021: ORIENT-31: Phase III study of sintilimab with or without IBI305 plus chemotherapy in patients with EGFR mutated non squamous NSCLC who progressed after EGFR-TKI therapy. ESMO Virtual Plenary Abstract. 2022 Jan; 33 (1): 112-113

  BACKGROUND

• Yip PY. Phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin (PI3K-Akt-mTOR) signaling pathway in non-small cell lung cancer. Transl Lung Cancer Res. 2015 Apr;4(2):165-76. doi: 10.3978/j.issn.2218-6751.2015.01.04.

  PMID: 25870799 BACKGROUND

• Yang JC, Robichaux J, Planchard D, Kobayashi K, Lee CK, Sugawara S, et al. FLAURA2: Resistance, and Impact of Baseline TP53 Alterations in Patients Treated With 1L Osimertinib ± Platinum-Pemetrexed. 2024 WCLC. Abstract MA12.03

  BACKGROUND

• Wang W, Li J, Ma S, Li H, Gao Z, Qu M. EGFR TKIs Combinding the inhibition of RAS-ERK signaling in NSCLC Treatment. J Clin Res Oncol 2021; 4(1): 1-9

  BACKGROUND

• Wang J, Wang B, Chu H, Yao Y. Intrinsic resistance to EGFR tyrosine kinase inhibitors in advanced non-small-cell lung cancer with activating EGFR mutations. Onco Targets Ther. 2016 Jun 22;9:3711-26. doi: 10.2147/OTT.S106399. eCollection 2016.

  PMID: 27382309 BACKGROUND

• Vokes NI, Le X, Yap TA. PIKing up and AKTing on Resistance Mutations in Osimertinib-Treated EGFR-Mutated NSCLC. Clin Cancer Res. 2024 Sep 13;30(18):3968-3970. doi: 10.1158/1078-0432.CCR-24-1188.

  PMID: 39018064 BACKGROUND

• Soria JC, Ohe Y, Vansteenkiste J, Reungwetwattana T, Chewaskulyong B, Lee KH, Dechaphunkul A, Imamura F, Nogami N, Kurata T, Okamoto I, Zhou C, Cho BC, Cheng Y, Cho EK, Voon PJ, Planchard D, Su WC, Gray JE, Lee SM, Hodge R, Marotti M, Rukazenkov Y, Ramalingam SS; FLAURA Investigators. Osimertinib in Untreated EGFR-Mutated Advanced Non-Small-Cell Lung Cancer. N Engl J Med. 2018 Jan 11;378(2):113-125. doi: 10.1056/NEJMoa1713137. Epub 2017 Nov 18.

  PMID: 29151359 BACKGROUND

• Sirico M, D'Angelo A, Gianni C, Casadei C, Merloni F, De Giorgi U. Current State and Future Challenges for PI3K Inhibitors in Cancer Therapy. Cancers (Basel). 2023 Jan 23;15(3):703. doi: 10.3390/cancers15030703.

  PMID: 36765661 BACKGROUND

• Reck M, Popat S, Reinmuth N, De Ruysscher D, Kerr KM, Peters S; ESMO Guidelines Working Group. Metastatic non-small-cell lung cancer (NSCLC): ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2014 Sep;25 Suppl 3:iii27-39. doi: 10.1093/annonc/mdu199. Epub 2014 Aug 11. No abstract available.

  PMID: 25115305 BACKGROUND

• Goldstein P. The synaptonemal complexes of Caenorhabditis elegans: pachytene karyotype analysis of hermaphrodites from the recessive him-5 and him-7 mutants. J Cell Sci. 1986 Jun;82:119-27. doi: 10.1242/jcs.82.1.119.

  PMID: 3793776 BACKGROUND

• Passaro A, Wang J, Wang Y, Lee SH, Melosky B, Shih JY, Wang J, Azuma K, Juan-Vidal O, Cobo M, Felip E, Girard N, Cortot AB, Califano R, Cappuzzo F, Owen S, Popat S, Tan JL, Salinas J, Tomasini P, Gentzler RD, William WN Jr, Reckamp KL, Takahashi T, Ganguly S, Kowalski DM, Bearz A, MacKean M, Barala P, Bourla AB, Girvin A, Greger J, Millington D, Withelder M, Xie J, Sun T, Shah S, Diorio B, Knoblauch RE, Bauml JM, Campelo RG, Cho BC; MARIPOSA-2 Investigators. Amivantamab plus chemotherapy with and without lazertinib in EGFR-mutant advanced NSCLC after disease progression on osimertinib: primary results from the phase III MARIPOSA-2 study. Ann Oncol. 2024 Jan;35(1):77-90. doi: 10.1016/j.annonc.2023.10.117. Epub 2023 Oct 23.

  PMID: 37879444 BACKGROUND

• NMPA approval of Capivasertib

  BACKGROUND

• Mok T, Nakagawa K, Park K, Ohe Y, Girard N, Kim HR, Wu YL, Gainor J, Lee SH, Chiu CH, Kim SW, Yang CT, Wu CL, Wu L, Lin MC, Samol J, Ichikado K, Wang M, Zhang X, Sylvester J, Li S, Forslund A, Yang JC. Nivolumab Plus Chemotherapy in Epidermal Growth Factor Receptor-Mutated Metastatic Non-Small-Cell Lung Cancer After Disease Progression on Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors: Final Results of CheckMate 722. J Clin Oncol. 2024 Apr 10;42(11):1252-1264. doi: 10.1200/JCO.23.01017. Epub 2024 Jan 22.

  PMID: 38252907 BACKGROUND

• Marrocco I, Yarden Y. Resistance of Lung Cancer to EGFR-Specific Kinase Inhibitors: Activation of Bypass Pathways and Endogenous Mutators. Cancers (Basel). 2023 Oct 16;15(20):5009. doi: 10.3390/cancers15205009.

  PMID: 37894376 BACKGROUND

• Middleton G, Fletcher P, Popat S, Savage J, Summers Y, Greystoke A, Gilligan D, Cave J, O'Rourke N, Brewster A, Toy E, Spicer J, Jain P, Dangoor A, Mackean M, Forster M, Farley A, Wherton D, Mehmi M, Sharpe R, Mills TC, Cerone MA, Yap TA, Watkins TBK, Lim E, Swanton C, Billingham L. The National Lung Matrix Trial of personalized therapy in lung cancer. Nature. 2020 Jul;583(7818):807-812. doi: 10.1038/s41586-020-2481-8. Epub 2020 Jul 15.

  PMID: 32669708 BACKGROUND

• Lynch JT, McEwen R, Crafter C, McDermott U, Garnett MJ, Barry ST, Davies BR. Identification of differential PI3K pathway target dependencies in T-cell acute lymphoblastic leukemia through a large cancer cell panel screen. Oncotarget. 2016 Apr 19;7(16):22128-39. doi: 10.18632/oncotarget.8031.

  PMID: 26989080 BACKGROUND

• Leonetti A, Sharma S, Minari R, Perego P, Giovannetti E, Tiseo M. Resistance mechanisms to osimertinib in EGFR-mutated non-small cell lung cancer. Br J Cancer. 2019 Oct;121(9):725-737. doi: 10.1038/s41416-019-0573-8. Epub 2019 Sep 30.

  PMID: 31564718 BACKGROUND

• Jacobsen K, Bertran-Alamillo J, Molina MA, Teixido C, Karachaliou N, Pedersen MH, Castellvi J, Garzon M, Codony-Servat C, Codony-Servat J, Gimenez-Capitan A, Drozdowskyj A, Viteri S, Larsen MR, Lassen U, Felip E, Bivona TG, Ditzel HJ, Rosell R. Convergent Akt activation drives acquired EGFR inhibitor resistance in lung cancer. Nat Commun. 2017 Sep 4;8(1):410. doi: 10.1038/s41467-017-00450-6.

  PMID: 28871105 BACKGROUND

• Holland WS, Chinn DC, Lara PN Jr, Gandara DR, Mack PC. Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines. J Cancer Res Clin Oncol. 2015 Apr;141(4):615-26. doi: 10.1007/s00432-014-1855-4. Epub 2014 Oct 17.

  PMID: 25323938 BACKGROUND

• Grazini U, Markovets A, Ireland L, O'Neill D, Phillips B, Xu M, Pfeifer M, Vaclova T, Martin MJ, Bigot L, Friboulet L, Hartmaier R, Cuomo ME, Barry ST, Smith PD, Floc'h N. Overcoming Osimertinib Resistance with AKT Inhibition in EGFRm-Driven Non-Small Cell Lung Cancer with PIK3CA/PTEN Alterations. Clin Cancer Res. 2024 Sep 13;30(18):4143-4154. doi: 10.1158/1078-0432.CCR-23-2540.

  PMID: 38630555 BACKGROUND

• Globocan 2022

  BACKGROUND

• Gris-Oliver A, Palafox M, Monserrat L, Braso-Maristany F, Odena A, Sanchez-Guixe M, Ibrahim YH, Villacampa G, Grueso J, Pares M, Guzman M, Rodriguez O, Bruna A, Hirst CS, Barnicle A, de Bruin EC, Reddy A, Schiavon G, Arribas J, Mills GB, Caldas C, Dienstmann R, Prat A, Nuciforo P, Razavi P, Scaltriti M, Turner NC, Saura C, Davies BR, Oliveira M, Serra V. Genetic Alterations in the PI3K/AKT Pathway and Baseline AKT Activity Define AKT Inhibitor Sensitivity in Breast Cancer Patient-derived Xenografts. Clin Cancer Res. 2020 Jul 15;26(14):3720-3731. doi: 10.1158/1078-0432.CCR-19-3324. Epub 2020 Mar 27.

  PMID: 32220884 BACKGROUND

• Fruman DA, Rommel C. PI3K and cancer: lessons, challenges and opportunities. Nat Rev Drug Discov. 2014 Feb;13(2):140-56. doi: 10.1038/nrd4204.

  PMID: 24481312 BACKGROUND

• Fei SJ, Zhang XC, Dong S, Cheng H, Zhang YF, Huang L, Zhou HY, Xie Z, Chen ZH, Wu YL. Targeting mTOR to overcome epidermal growth factor receptor tyrosine kinase inhibitor resistance in non-small cell lung cancer cells. PLoS One. 2013 Jul 16;8(7):e69104. doi: 10.1371/journal.pone.0069104. Print 2013.

  PMID: 23874880 BACKGROUND

• Dunn S, Eberlein C, Yu J, Gris-Oliver A, Ong SH, Yelland U, Cureton N, Staniszewska A, McEwen R, Fox M, Pilling J, Hopcroft P, Coker EA, Jaaks P, Garnett MJ, Isherwood B, Serra V, Davies BR, Barry ST, Lynch JT, Yusa K. AKT-mTORC1 reactivation is the dominant resistance driver for PI3Kbeta/AKT inhibitors in PTEN-null breast cancer and can be overcome by combining with Mcl-1 inhibitors. Oncogene. 2022 Nov;41(46):5046-5060. doi: 10.1038/s41388-022-02482-9. Epub 2022 Oct 14.

  PMID: 36241868 BACKGROUND

• De Marco C, Malanga D, Rinaldo N, De Vita F, Scrima M, Lovisa S, Fabris L, Carriero MV, Franco R, Rizzuto A, Baldassarre G, Viglietto G. Mutant AKT1-E17K is oncogenic in lung epithelial cells. Oncotarget. 2015 Nov 24;6(37):39634-50. doi: 10.18632/oncotarget.4022.

  PMID: 26053093 BACKGROUND

• Davies BR, Greenwood H, Dudley P, Crafter C, Yu DH, Zhang J, Li J, Gao B, Ji Q, Maynard J, Ricketts SA, Cross D, Cosulich S, Chresta CC, Page K, Yates J, Lane C, Watson R, Luke R, Ogilvie D, Pass M. Preclinical pharmacology of AZD5363, an inhibitor of AKT: pharmacodynamics, antitumor activity, and correlation of monotherapy activity with genetic background. Mol Cancer Ther. 2012 Apr;11(4):873-87. doi: 10.1158/1535-7163.MCT-11-0824-T. Epub 2012 Jan 31.

  PMID: 22294718 BACKGROUND

• Chen Y, Huang L, Dong Y, Tao C, Zhang R, Shao H, Shen H. Effect of AKT1 (p. E17K) Hotspot Mutation on Malignant Tumorigenesis and Prognosis. Front Cell Dev Biol. 2020 Oct 6;8:573599. doi: 10.3389/fcell.2020.573599. eCollection 2020.

  PMID: 33123537 BACKGROUND

• Chen X, Zhang D, Xue J, Li Z. Selective targeting of the AKT1 (E17K) mutation: advances in precision oncology and therapeutic design. Discov Oncol. 2025 Jul 3;16(1):1257. doi: 10.1007/s12672-025-03083-0.

  PMID: 40608215 BACKGROUND

• Chen P, Liu Y, Wen Y, Zhou C. Non-small cell lung cancer in China. Cancer Commun (Lond). 2022 Oct;42(10):937-970. doi: 10.1002/cac2.12359. Epub 2022 Sep 8.

  PMID: 36075878 BACKGROUND

• Bokobza SM, Jiang Y, Weber AM, Devery AM, Ryan AJ. Combining AKT inhibition with chloroquine and gefitinib prevents compensatory autophagy and induces cell death in EGFR mutated NSCLC cells. Oncotarget. 2014 Jul 15;5(13):4765-78. doi: 10.18632/oncotarget.2017.

  PMID: 24946858 BACKGROUND

• Bertoli E, De Carlo E, Del Conte A, Stanzione B, Revelant A, Fassetta K, Spina M, Bearz A. Acquired Resistance to Osimertinib in EGFR-Mutated Non-Small Cell Lung Cancer: How Do We Overcome It? Int J Mol Sci. 2022 Jun 22;23(13):6936. doi: 10.3390/ijms23136936.

  PMID: 35805940 BACKGROUND

• Choudhury NJ, Marra A, Sui JSY, Flynn J, Yang SR, Falcon CJ, Selenica P, Schoenfeld AJ, Rekhtman N, Gomez D, Berger MF, Ladanyi M, Arcila M, Rudin CM, Riely GJ, Kris MG, Heller G, Reis-Filho JS, Yu HA. Molecular Biomarkers of Disease Outcomes and Mechanisms of Acquired Resistance to First-Line Osimertinib in Advanced EGFR-Mutant Lung Cancers. J Thorac Oncol. 2023 Apr;18(4):463-475. doi: 10.1016/j.jtho.2022.11.022. Epub 2022 Dec 6.

  PMID: 36494075 BACKGROUND

Related Links

• Chinese Society of Clinical Oncology. Non-small Cell Lung Cancer. 2025.
• GLOBOCAN 2022

MeSH Terms

Conditions

Lung Neoplasms; Carcinoma, Non-Small-Cell Lung

Interventions

capivasertib; osimertinib

Condition Hierarchy (Ancestors)

Respiratory Tract Neoplasms; Thoracic Neoplasms; Neoplasms by Site; Neoplasms; Lung Diseases; Respiratory Tract Diseases; Carcinoma, Bronchogenic; Bronchial Neoplasms

Central Study Contacts

Jie Wang

CONTACT

+86-0351-4881611; 15234165176@163.com

Study Design

• Study Type: interventional
• Phase: phase 1
• Allocation: NA
• Masking: NONE
• Purpose: TREATMENT
• Intervention Model: SEQUENTIAL
• Sponsor Type: OTHER
• Responsible Party: SPONSOR

Model Details: The study includes 2 parts:Part A:Dose escalation; Part B:Dose expansion

Study Record Dates

• First Submitted: February 25, 2026
• First Posted: March 20, 2026
• Study Start: May 15, 2026
• Primary Completion (Estimated): October 15, 2028
• Study Completion (Estimated): December 31, 2028
• Last Updated: March 24, 2026

Record last verified: 2026-03

Data Sharing

• IPD Sharing: Will not share

Locations

CN (2)