VRN11 is an orally available targeted therapy for lung cancer currently in development, designed as a selective inhibitor targeting EGFR mutations.
VRN11 has demonstrated activity against both common EGFR mutations, including Del19 and L858R, as well as uncommon EGFR mutations. In addition, it targets C797S, a key resistance mutation associated with current EGFR-targeted therapies.

Due to its high selectivity, VRN11 has demonstrated a favorable safety profile while maintaining encouraging anti-tumor activity.
In one patient treated at the 40mg dose level, a 22.2mm lung tumor was reduced by more than 50% after two months of treatment.
In addition, no significant treatment-related toxicities have been reported to date, even at doses up to 480mg, which is 12-fold higher than the effective 40mg dose.

Given the high incidence of CNS metastases in lung cancer patients, there remains a significant unmet medical need for therapies with effective blood-brain barrier (BBB) penetration.
VRN11 has demonstrated strong BBB penetration, with a patient-confirmed Kp,uu, CSF value of 2.0, indicating substantially higher unbound drug exposure in the CNS compared to plasma. This level is approximately 10-fold higher than the reported value for Tagrisso (0.2).
In addition, multiple complete responses (CRs) have been observed in patients with brain metastases, and VRN11 has demonstrated encouraging activity against CNS metastases, including brain metastases (BM) and leptomeningeal metastases (LM).

The Phase 1a clinical trial is currently ongoing in patients with diverse EGFR-mutant lung cancers who have exhausted available treatment options.
Pharmacokinetic analyses have demonstrated dose-proportional increases in unbound plasma exposure with escalating doses of VRN11. In addition, anti-tumor activity was observed in 30 of 31 patients who had previously received two or more lines of therapy (DCR 96.8% [30/31]).
As a 4th-generation EGFR-targeted therapy, VRN11 was designed with the goal of achieving improved efficacy and safety compared to current 3rd-generation therapies, including Tagrisso. We plans to further evaluate its clinical potential through ongoing and future clinical studies.

For more detailed information, please refer to the poster below.

VRN10 is an orally bioavailable, HER2-selective targeted therapy currently being evaluated in a Phase 1a clinical trial. Due to its high selectivity, VRN10 has demonstrated encouraging anti-tumor activity while maintaining a favorable safety profile.

The Phase 1a clinical trial is ongoing in patients with various HER2-positive solid tumors who have exhausted available treatment options.
VRN10 has demonstrated activity against a broad range of HER2 mutations, as well as tumors driven by HER2 amplification and overexpression.

Specifically, in patients with HER2 mutations, the ORR was 43% (3/7) and the DCR was 86% (6/7). Tumor reduction was observed across multiple HER2 mutation subtypes, including S310F, S310Y, V659E, V777L, and L755P.

In HER2-positive breast cancer, the ORR was 17% (1/6) and the DCR was 83% (5/6). All patients in this cohort had received trastuzumab deruxtecan (T-DXd, Enhertu) as their most recent prior therapy before enrollment.
Given the limited treatment options and generally poor clinical outcomes in patients previously treated with T-DXd, these results represent an encouraging early efficacy signal in an area of high unmet medical need.

Despite its encouraging efficacy, no serious off-target adverse events have been observed to date. On-target adverse events, which are well known to be predictable and reversible, were found to be manageable, supporting a favorable tolerability profile.

Given the high incidence of CNS metastases in breast cancer patients, there remains a significant unmet medical need for therapies with effective BBB penetration.
In preclinical brain metastasis models, VRN10 demonstrated strong CNS penetration and superior anti-tumor activity compared with multiple HER2-targeted therapies, including Tucatinib, Neratinib, Zongertinib, Perzebertinib (ZN-A-1041), Trastuzumab, and Enhertu.

VRN10 has been developed to address unmet needs associated with existing HER2-targeted therapies, aiming to achieve improved efficacy and tolerability. Further clinical evaluation is ongoing to establish its therapeutic potential.

For more details, please refer to the poster below.

Partner

VRN16 is a novel selective orally available investigational drug that targets cancer cell’s vulnerability through a synthetic lethality mechanism including CCNE1-driven cancers.
CCNE1 amplification is found in approximately 8% of all solid tumors and is particularly prevalent in over 30% of ovarian and uterine cancers, 14% of gastric cancers, and 8% of breast cancers. Despite its role as a key oncogenic driver, no targeted therapies have been approved to date and remain an unmet medical need.
VRN16 is differentiated with markedly improved selectivity, tolerability, and anti-tumor activity in preclinical studies. With its differentiated profile, VRN16 may become a promising solution to patients with CCNE1-driven cancers.
New indications are explored based on novel biomarkers specific to PKMYT1 inhibition.

VRN19 is a best-in-class orally available USP1 inhibitor that leverages the mechanism of synthetic lethality to selectively target BRCA1/2 mutated cancers, including ovarian and breast cancers, as well as other solid tumors.
Unlike competing USP1 inhibitors, which have shown limitations in tolerability and efficacy due to hematologic toxicity (e.g., anemia) and hepatotoxicity, VRN19 demonstrates excellent tolerability and potent antitumor activity, offering a broad therapeutic window.
In addition to its current indications, biomarker research is also underway to explore potential expansion into new therapeutic areas.

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VRN13 is a best-in-class inhalation therapy in development for the treatment of pulmonary arterial hypertension (PAH).

Direct delivery to the lungs is anticipated to reduce systemic exposure and provide superior safety and efficacy over current therapies.
PAH is a rare disease characterized by abnormal elevation of pulmonary arterial pressure due to vascular remodeling in the pulmonary vasculature and no curative therapies are available to date. Among various pathological pathways, the PDGFR signaling pathway is well known as a key player in vascular remodeling and has emerged as a promising therapeutic target.
Imatinib(Gleevec), a known PDGFR inhibitor, demonstrated meaningful clinical efficacy in the Phase 3 IMPRES trial. However, its systemic administration led to neurological adverse events, which ultimately led to the discontinuation of its clinical development.
To overcome these limitations, VRN13 has been designed as an inhalation therapy that enables localized drug exposure to the pulmonary vasculature. Also, high selectivity for PDGFR and low inhibitory activity against VEGFR-2 (minimizing vascular-related side effects), contributes to an improved safety profile.
With its differentiated mechanism and targeted delivery, VRN13 has the potential to emerge as a globally competitive and best-in-class therapy for PAH.