1. Clear MoA.
1)TIM3 is an inhibitory immune checkpoint that is expressed on the surface of T cells, DCs, Treg cells and other innate immune cells, and can cause T cell exhaustion and tumor immune escape.
2)Patients with TIM3 overexpressing show ineffective anti-PD1 therapy.
3)Dual-blockade of TIM3 and PD1 can significantly activate antitumor effects.
2. TIM3 × PD1 bsAb is the first to simultaneously release the inhibitory activity of DCs, T cells, and NK cells.
1) Significantly activate the tumor-killing activity of NK cells
2) Restore DCs antigen-presenting ability and T cells tumor-killing activity
3. high binding affinity.
1) Anti-PD-1 effect in liver cancer is comparable to Keytruda（77-88%TGI）;
2) Anti-TIM3 ability is stonger than RG7769;
3) Anti-TIM3 ability of the BsAb is comparable to anti-PD-1（approximated 5-8nM）.
4. BsAb shows high antitumor activity in PD1 insensitive mouse model and at the day 40 the survival ratio reachs to 85% which is superior to a combination of anti-TIM3 and anti-PD1 due to synergistic effects.
5. Good PK/PD property.
1) HNSTD=200 mpk;
2) At the dose of 2、10、50 mpk，ADA=33.3%(2/6)、83.3%(5/6)and 0.0%(0/6);
3) At the dose of 2-50 mpk，t1/2=31.7-66.5 h.
1. Asset type: TIM3×PD-1 bsAb
2. Indication: Solid Tumor
4. Research phase: Phase 1
5. Cooperation demands: License-out or co-development
6. Research progress：
1) Got document for clinical trials in China and USA, Phase Ⅰ in China and have plans of second or third treatment for NSCLC(10 patients).
2) The pre-clinical data is more competitive than other products in clinical.
3) Inhibit tumor growth in PD-1 insensitive model, prolong survival ratio and its effectiveness is better than solitary drug or combination.
4) Good safety and PK/PD property.
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