Exhibit 99.1

Professor Mark W Lowdell CSO 1 “Exploring the cellular interactions between NK cells, tumor cells and the TME”

Tumor - derived Inhibitory signals Activating signals Tumor - derived Inhibitory signals Activating signals Tumor - derived Inhibitory signals Activating signals Activating signals Activating signals NK - Tumor TROGOCYTOSIS NK - NK interactions % of conjugates NK-NK cells 0 20 40 60 80 0.0 0.5 1.0 1.5 2.0 NK:K562[1:5] NK:K562[1:1] NK:K562[5:1] Time[min] % of conjugates

• Balance of signals – Tumor “sensitivity” • NK:tumor cell ratio • NK cell subset • Prior exposure? – TiM - NK – CiM - NK • Inhibitory microenvironment What determines the outcome of NK - tumor ligation? CD15 - ve K562 NK resistant rNK cell X rNK lack enough activating signals to overcome tumor inhibition

E:T determines outcome Low E:T ratios = High NK activation and degranulation – Low lysis CD107a expression on NK cells K 5 6 2 I N B 1 6 0 20 40 60 80 rNK NK+Target[1:2] NK+Target[2:1] NK+Target[5:1] NK+Target[10:1] % o f e x p r e s s i o n CD69 expression on NK cells K 5 6 2 I N B 1 6 0 20 40 60 80 rNK NK+Target[1:2] NK+Target[2:1] NK+Target[5:1] NK+Target[10:1] % o f e x p r e s s i o n NK mediated lysis K 5 6 2 I N B 1 6 0 20 40 60 80 100 NK+Target[1:2] NK+Target[2:1] NK+Target[5:1] NK+Target[10:1] % o f s p e c i f i c l y s i s CD69 expression after 4h on NK subpopulations rNK NK:INB16 [1:2]NK:INB16 [2:1]NK:INB16 [5:1]NK:INB16 [10:1] 0 20 40 60 80 100 CD107a(-) with monensin CD107a(+) with monensin CD107a(-) w/o monensin CD107a(+) w/o monensin % of expression

Prior exposure to tumor cells may impair or enhance tumor killing Priming effect % of expression on NK cells TNFa IFNy Perforin GranzymeB 0 5 10 15 50 60 70 80 90 100 rNK NK+K562 [1:2] NK+INB16 [1:2] % of expression

NK - NK activation following trogocytosis C D 6 9 0 20 40 60 rNK +TpNK +IL15[1ng/mL] % r N K r e c e p t o r e x p r e s s i o n +TpNK(1:10)+IL15 rNK priming by TpNK

CD107a expression on NK cells r N K N K + [ K 5 6 2 ] N K + [ K 5 6 2 2 4 h ] N K + [ K 5 6 2 l y s a t e s ] N K + [ I N B 1 6 ] N K + [ I N B 1 6 2 4 h ] N K + [ I N B 1 6 l y s a t e s ] 0 20 40 60 80 % o f e x p r e s s i o n Killing assay for Raji cells r N K + T a r g e t N K + [ K 5 6 2 ] + T a r g e t N K + [ K 5 6 2 2 4 h ] + T a r g e t N K + [ K 5 6 2 l y s a t e s ] + T a r g e t N K + [ I N B 1 6 ] + T a r g e t N K + [ I N B 1 6 2 4 h ] + T a r g e t N K + [ I N B 1 6 l y s a t e s ] + T a r g e t 0 20 40 60 80 % o f s p e c i f i c l y s i s NK cells are activated by tumor cell membranes but do not express CD69 or degranulate Expression on NK cells C D 6 9 C D 1 6 0 20 40 60 80 100 rNK NK+[K562] NK+[K562 24h] NK+[K562 lysates] NK+[INB16] NK+[INB16 24h] NK+[INB16 lysates] % o f e x p r e s s i o n

Does tumor exposure influence NK avidity? Kushal Kumar Das - Lumicks Acoustic Node Glass 0.1mm Piezo Element Target tumor cells Primed vs Resting NK cells Ultrasound is used to exert forces completely contactless to NK cells in a microfluidic chip

CD107a expression on NK cells rNK NK+K562[1:2]NK+INB16[1:2] 0 20 40 60 80 100 % of expression Killing assay: % of specific lysis (after 4h) NK+K562 [5:1] NK+INB16 [5:1] 0 20 40 60 80 100 % of specific lysis

Data by Amanda van Vliet CAR - NK Mock - NK 90% lysis 30% lysis

CD107a expression on NK cells rNK NK+K562[1:2]NK+INB16[1:2] 0 20 40 60 80 100 % of expression Killing assay: % of specific lysis (after 4h) NK+K562 [5:1] NK+INB16 [5:1] 0 20 40 60 80 100 % of specific lysis E:T [1:1] 15min 30min 45min 60min 0 5 10 rNK TpNK LAK % of conjugates

Alive >2yrs % K562 lysis NK function only needs to be “adequate”

Effects of hypoxia may be transient and tumor cell dependent 4 6 16 0 20 40 60 80 100 NK NK (hyp) Time (h) S p e c i f i c C y t o l y s i s ( % ) K562 + rNK RAJI +LAK15 4 6 16 24 48 0 20 40 60 80 100 Time (h) S p e c i f i c C y t o l y s i s ( % ) NK+IL15(10ng/ml) NK+IL15(10ng/ml (hyp) 4 6 16 24 48 0 20 40 60 80 100 Time (h) S p e c i f i c C y t o l y s i s ( % ) NK NK (hyp) OVCAR3 + rNK OVCAR3 +LAK15 4 6 16 0 20 40 60 80 100 Time (h) S p e c i f i c C y t o l y s i s ( % ) Raji+TpNK Raji+TpNK (hyp) 4 6 16 0 20 40 60 80 100 Time (h) S p e c i f i c C y t o l y s i s ( % ) Raji+NK+IL-15 (10ng) O/N Raji+NK+IL-15 (10ng) O/N (hyp) 4 6 16 24 48 0 20 40 60 80 100 Time (h) S p e c i f i c C y t o l y s i s ( % ) TpNK TpNK (hyp) OVCAR3 + TpNK RAJI + TpNK

Effects of inhibitory cells in the TME Myeloid - derived suppressor cells Treg Suppression of MLR T r e g : T c o n v 1 : 2 T r e g : T c o n v 1 : 4 T r e g : T c o n v 1 : 8 T r e g : T c o n v 1 : 1 6 T r e g : T c o n v 1 : 3 2 0 20 40 60 80 % o f s u p p r e s s i o n S p e c i f c i c y t o l y s i s N K + R A J I N K + T r e g + R A J I N K + I L 2 1 0 0 I U + R A J I N K + T r e g + I L 2 1 0 0 I U + R A J I T p N K + R A J I   T p N K + T r e g + R A J I 0 20 40 60 80 100 Treg Suppression of NK-mediated lysis K562 lysis 5:1:1 0 20 40 60 80 100 rNK rNK:CD33 (IL-6) Allo 1 rNK:CD33 (VEGF) Allo 1 rNK:CD33 (IL-6) Allo 2 rNK:CD33 (VEGF) Allo 2 rNK:CD33 (IL-6) Auto rNK:CD33 (VEGF) Auto % o f s p e c i f i c l y s i s K562 lysis 5:1:1 0 10 20 30 40 % C D 1 0 7 a + Allo 1 Allo 2 AutoNIL

Conclusions • NK:tumor cell interactions are multicellular and multifactorial • Degranulation is not a direct correlate of lysis and thus not of exhaustion • Tumor cell conjugation may induce activation without lysis and generate a primed state associated with increased TNF - a and IFN - g and increased avidity to secondary tumor targets • Classical regulatory factors in the TME can inhibit NK function in vitro but the effects are transient and may be overcome by appropriate activating signals • Increased avidity enhances lysis but not conjugation duration and may be a tool to develop, screen and qualify novel NK activating agents • The molecular basis of increased avidity is being dissected