VRN11 is an oral, targeted therapy for lung cancer currently in development, designed as a selective agent for EGFR mutations. It is effective not only against typical (Common) mutations, such as EGFR Del19 and L858R, but also against atypical (Uncommon) mutations. Furthermore, it is effective against C797S, a key mutation that confers resistance to existing treatments.

Due to its high selectivity, VRN11 demonstrates an excellent safety profile despite its outstanding efficacy. In a patient treated with a 40mg dose, a 22.2mm lung tumor was reduced by over 50% in just two months. Furthermore, no drug-related side effects have been observed thus far, even at 400mg, a 10-fold higher dose.

Given that 80% of lung cancer patients are known to develop brain metastases within two years, there is a significant unmet medical need for drugs that can penetrate the blood-brain barrier (BBB). VRN11 exhibits high BBB penetration. The Kp,uu, CSF value confirmed in patients is 2.0, indicating that the drug concentration in the brain is twice as high as in the blood. This is 10-fold higher than Tagrisso's 0.2 Multiple Complete Responses (CR) have been confirmed in patients with brain metastases. Among 11 patients with Brain Metastasis

(BM) or Leptomeningeal Metastasis (LM) treated at doses of 160mg or higher, all demonstrated anti-tumor effects (DCR 100% [11/11]).
The Phase 1a trial is currently underway in patients with diverse EGFR-mutant lung cancer who have no further treatment options. It has been confirmed that as the patient dose increases, the free drug concentration in the blood increases proportionally. Additionally, anti-tumor effects were observed in 20 out of 21 patients who had previously received two or more lines of anti-cancer therapy (DCR 95.2% [20/21]).
As a 4th-generation drug, VRN11 was developed with the goal of achieving superior efficacy and safety compared to 3rd-generation drugs (like Tagrisso). We plan to prove its value through future clinical trials.
For more detailed information, please refer to the poster below.

VRN10 is an orally bioavailable, HER2-selective targeted therapy currently in Phase 1a clinical trial. It demonstrates potent activity against a range of HER2 mutations as well as cancers driven by HER2 amplification and overexpression.

Due to its high selectivity, VRN10 demonstrates excellent efficacy while maintaining a favorable safety profile.
We observed antitumor activity of VRN10 in HER2-positive solid tumors starting from the initial Phase 1a dose of 80 mg. In a patient with pancreatic cancer (HER2 S310F mutation), the tumor shrank by 26.7% after only three weeks of treatment. In a patient with gastric cancer (HER2 IHC 2+/DISH-), rapid tumor growth was halted after four weeks, resulting in stable disease.
At the second dose level of 160 mg, a patient with lung cancer (HER2 S310Y) who had metastases to the breast and liver achieved a complete disappearance of the lung lesion and a 28.6% reduction in the metastatic breast and liver tumors after six weeks of treatment. Similarly, a patient with breast cancer (HER2 V777L) experienced a 24.2% reduction in two metastatic liver lesions.
Despite its remarkable efficacy, no serious adverse events have been observed to date.

The Phase 1a clinical trial is ongoing in patients with various HER2-positive solid tumors who have no remaining treatment options. Among the two patients who showed tumor responses at 160 mg, one had previously received seven and the other five different anticancer regimens. Their most recent prior treatment before entering the trial was Enhertu (T-DXd).
We have established cancer cell models resistant to Enhertu (T-DXd) and confirmed the efficacy of VRN-10 through both in vitro and in vivo studies.

Because breast cancer has a high incidence of brain metastases, there remains a significant unmet medical need for agents that can effectively penetrate the blood–brain barrier (BBB). VRN-10 demonstrates high BBB permeability, and in preclinical brain metastasis models, it showed superior antitumor efficacy compared with Tucatinib, Neratinib, Zongertinib, Perzebertinib (ZN-A-1041), Trastuzumab, and Enhertu.

VRN10 has been developed with the goal of overcoming the various limitations of existing HER2-targeted therapies, aiming to achieve both exceptional efficacy and a favorable safety profile. Its therapeutic value will be further validated through ongoing and future clinical studies.
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.

Partner

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.