Highlights

1. Clear MoA.

(1) CLDN 18.2 is a tight-junction protein, and typically buried in gastric mucosa. Anti-CLDN 18.2 macromolecular drugs can not bind to it due to cell tight junction function in normal tissues.

(2) CLDN 18.2 is highly expressed in some cancer, such as gastric cancer, pancreatic cancer. And these cancer cells’ connection is so loose that anti-CLDN 18.2 mAb can bind to it.

(3) CLDN 18.2 is a promising target among HER-2 negative gastric cancer patients, not only on high selectivity, but also on population prevalence.

2. Excellent preclinical efficacy:

(1) Cross with human, mouse, monkeys.

(2) CLDN 18.2 mAb had high affinity in vitro. It is more effective than IMAB362 in many cancer cell models.

(3) High affinity in vivo.

(4) Excellent safety: MTD = 400 mg/kg, HNSTD = 100 mg/kg in monkeys. No dose-dependent AEs have been identified in monkeys and mouse. Plasma cytokine concentrations(IFNγ, TNFα, IL6, IL10, IL2 ) were not abnormally increased after mAb administration.

3. Excellent PhaseⅠclinical result:

CLDN 18.2 mAb was well-tolerated for the 0.3mg/kg through 20mg/kg Q3W as no DLTs were observed.

4. Good market potential:

It is estimated that the number of new pancreatic cancer patients worldwide will reach 486,300 in 2028, and the pancreatic cancer drug market will reach US$4.1 billion; the global new gastric cancer patients will reach 1.1 million, and the gastric cancer drug market will reach US$4.4 billion.

Research progress：

(1) Completed preclinical development

(2) Phase I clinical trials are ongoing to evaluate the safety, tolerability, pharmacokinetics and efficacy of candidate antibodies for advanced malignancies.