Jiangsu Vcare’s Next-Generation TRK Inhibitor Eratrectinib (VC004) Selected for the “SPARK Plan” for Pediatric Oncology Drugs

　　Recently, Eratrectinib (VC004), a next-generation TRK inhibitor independently developed by Jiangsu Vcare PharmaTech Co., Ltd. (Jiangsu Vcare), was included in the " Support Anti-tumor drugR&D for Kids (SPARK Plan)" launched by the CDE of the NMPA, become the 5th innovative drug variety in the country to be included in this program. This important progress will accelerate the R&D process of the domestic new anticancer drug Eratrectinib in the field of pediatric oncology, bringing new hope to pediatric oncology patients in China.

　　As a next-generation TRK inhibitor, Eratrectinib achieves superior efficacy compared with the first-generation TRK inhibitors while effectively addressing the drug resistance issues of the latter. In vitro kinase assays have shown that it exhibits excellent inhibitory effects on both wild-type and mutant TRK kinases.

　　Currently, the NDA for Eratrectinib in the treatment of solid tumors harboring NTRK fusion genes in adults and adolescents aged 12 years and above has been officially accepted and included in the priority review and approval process, with related initiatives proceeding as planned. Meanwhile, the Phase III clinical trial evaluating the safety and efficacy of Eratrectinib in patients with locally advanced/metastatic solid tumors is ongoing for patient enrollment. This study plans to include NTRK fusion-positive solid tumor patients, including children aged 2 to <12 years, which will provide important clinical evidence for the application of Eratrectinib in pediatric patients.

　　NTRK gene fusion is an oncogenic driver for various adult and pediatric tumors. Pediatric solid tumors with NTRK gene fusion can occur at any age, and the incidence rate is higher in children，comparing to adults. The incidence of gene fusion reaches 2.28% in children aged <5 years, and exceeds 90% in some pediatric tumors. Currently, there remains a significant unmet clinical need for tumor patients harboring NTRK fusion genes in clinical practice.

　　About the "SPARK Plan"

　　The "Support Anti-tumor drugR&D for Kids (SPARK Plan)" was launched by the CDE of the NMPA on May 29, 2025. It seeks early, tailored engagement with each company, providing hands-on guidance throughout R&D and regulatory review in lockstep. Based on the "patient-Centered Action for Rare diseases Encouragement (CARE Plan)", it is a pilot initiative carried out in the field of pediatric drug R&D. Targeting products intended for the development of pediatric oncology indications in China, the " SPARK Plan" encourages applicants to communicate with the CDE at an early stage by filling out and submitting the "Implementation Framework for the R&D of Pediatric Anticancer Drugs", so as to obtain corresponding guidance on technical issues during the research of their anticancer drugs in pediatric populations. Meanwhile, maintaining close communication with the CDE during the R&D process will ultimately improve the R&D efficiency of pediatric anticancer drugs and promote their early market launch to meet patient needs.

　　About Eratrectinib

　　Eratrectinib (VC004) is a Class I small molecule targeted anti-tumor innovative drug independently developed by Jiangsu Vcare. As a next-generation TRK inhibitor, it has demonstrated superior efficacy compared to first-generation drugs targeting the same mechanism in clinical settings and addresses the issue of acquired resistance associated with first-generation drugs. It holds promise for delivering longer survival benefits and improved quality of life for patients. Currently, all first-generation drugs targeting this mechanism in the Chinese market are imported and have not yet received full marketing approval; furthermore, no second-generation drugs targeting this mechanism have been approved in China. This highlights the significant unmet clinical need. Eratrectinib possesses the following differentiated advantages:

　　1. Unique Second-Generation Anti-Resistance Mechanism: Based on in vitro kinase assay results, Eratrectinib not only exhibits comparable inhibitory activity against wild-type TRK to first-generation drugs in the same class but also demonstrates activity against first-generation drug resistance mechanisms. Its inhibitory potency against TRK mutant kinases reaches the nM level.

　　2. Significant Efficacy in Both Treatment-Naïve and Pre-Treated Patients: Based on results from the single-arm, pivotal Phase II clinical study, Eratrectinib demonstrated a higher clinical ORR than first-generation drugs. It also achieved favorable therapeutic outcomes in TRK TKIs pre-treated patients, further validating the differentiated advantages identified during the drug discovery phase in clinical studies.

　　3. Improved Clinical Safety Profile: The incidence of Grade ≥3 TRAEs was significantly lower compared to other drugs targeting the same mechanism, with no fatal TRAEs reported.

　　In China, Eratrectinib has adopted a single-arm Phase II clinical trial as its pivotal study, with its NDA officially accepted and included in the priority review and approval process. In the US, its IND application has been approved by the FDA, positioning it as a potential global-leading next-generation TRK inhibitor.

　　About NTRK Fusion-Positive Solid Tumors

　　NTRK gene fusions have been identified as oncogenic drivers in both adult and pediatric patients with a wide range of solid tumors. The NTRK genes (NTRK1, NTRK2, and NTRK3) encode the TRKA, TRKB, and TRKC receptors of the TRK family. These fusions act as drivers in multiple cancers and are found across numerous solid tumor types. Currently, NTRK fusion inhibitors demonstrated remarkable efficacy in clinical practice, holding immense potential in the field of oncology. In China, NTRK gene fusion mutations are observed in prevalent cancer types such as lung cancer, colorectal cancer, breast cancer, and thyroid cancer, as well as in certain rare cancers, including secretory breast carcinoma and salivary gland secretory carcinoma.

　　Nat Rev Clin Oncol. 2018 Dec;15(12):731-747.