KAPITALMARKNADSPRESENTATION 23 MARS 2015 MICHAEL OREDSSON, VD

STABIL BAS OCH BETYDANDE UPPSIDA Bioinvent har en teknologiplattform som redan skapat stort värde har tre produkter på väg in i klinisk fas I/II har fokus på immunonkologi och erbjuder signifikant mervärde för patienter och partners från prekliniskt till kliniskt bolag under 2015 kraftig hävstång i värdeskapandet optimerar värde genom mjuk finansiering i tidig klinisk fas

AFFÄRSSTRATEGI Bevara värdet i kliniska nyckelprojekt Cancer Research UK genomför fas I/II-studie för BI-1206 och tillför BioInvent > 60 MSEK i värde Fördelaktig finansieringsmodell i fas II-studie för BI-505 genom samarbete med University of Pennsylvania BioInvent behåller värdet i båda projekten inför fas IIb TB-403 går direkt in i effektsökande barncancerstudie i ultraorphan-indikation Skapa värde i F.I.R.S.T. genom Treg/TAM-samarbeten med Big Pharma/Big Biotech BioInvent tillförs licensintäkter, resurser och kompetens Genererar mångfald av antikroppar/targets/applikationer och ger möjlighet till bibehållet värde för BioInvent Fokus på USA BioInvent är mycket aktivt i USA: vår forskning håller hög klass och väcker stort intresse hos ledande aktörer

AGENDA 1.Immunonkologi framtidens cancerterapi 2.Bioinvents verktyg för nya cancerterapier 3.Egna läkemedelsprojekt 4.Prekliniska projekt 5.Affärsmodell 6.Nyemission 7.Bioinvent på rätt plats vid rätt tidpunkt

IMMUNONKOLOGI FRAMTIDENS BEHANDLING AV CANCER ASCO CHICAGO MAJ 2014 78 KLINISKA PRÖVNINGAR >1 MILJARD USD (YERVOY) 5

ANTIKROPPSLÄKEMEDEL HJÄLPER IMMUNFÖRSVARET ATT DÖDA CANCERCELLER YER VOY Immunsystemet är kroppens mest kraftfulla och effektiva verktyg för att känna igen och bekämpa cancer. Monoklonala antikroppar fäster på målceller och hjälper immunförsvaret att döda cancerceller. Immuno-onkologiska antikroppsläkemedel har redan nått marknaden, men behovet av ytterligare terapier är enormt. Antikroppsläkemedel har dubbelt så hög chans att nå marknaden jämfört med traditionella substanser (small molecules).

BEHANDLING AV CANCER KIRURGI STRÅLBEHANDLING CELLGIFTER UNDERSTÖDJANDE BEHANDLING IMMUNONKOLOGI

BIOINVENTS VERKTYG FÖR NYA CANCERTERAPIER

BIOINVENT HITTAR RÄTT ANTIKROPPAR Agnas med celler från patienter F.I.R.S.T. BioInvents verktyg för att hitta rätt antikropp n-coder - BioInvents bibliotek med 20-30 miljarder antikroppar

F.I.R.S.T BIOINVENTS UNIKA METOD ATT HITTA RÄTT ANTIKROPP friska celler sjuka celler 1. Antikroppsbiblioteket screenas mot sjuka och friska celler 2. Vi identifierar de antikroppar som binder till sjuka celler 3. Dessa antikroppar testas in vitro för att se vilka som som ger den bästa effekten 4. De bästa antikropparna väljs ut och produceras i större mängd inför fortsatta tester 5. Dessa antikroppar testas i BioInvents sjukdomsrelaterade djurmodeller

2015 ETT TRANSFORMERANDE ÅR TRE PRODUKTER I KLINISK FAS I/II

BIOINVENTS FOKUSERAR PÅ CANCER F.I.R.S.T LÄKEMEDELSPROJEKT STATUS DISCOVERY RESEARCH FAS I FAS II FAS III BI-505 (Multipelt Myelom) BI-1206 (NHL) START H2 2015 TB-403 (Medulloblastom) START H2 2015 Treg (Regulatoriska T-celler) TAM (TumörAssocierade Makrofager) 12

BI-505 MULTIPELT MYELOM LIVSHOTANDE BLODCANCER MED UPPREPADE ÅTERFALL ANGREPPSPUNKT: ICAM-1 SOM PÅVERKAR IMMUNSYSTEMETS MAKROFAGER SYNERGI MED REVLIMID/VELCADE GOD SÄKERHET OCH DJUP RESPONS KAN HINDRA/FÖRDRÖJA ÅTERFALL START AV FAS IIA I STAMCELLS- TRANSPLANTERADE PATIENTER REVLIMID/VELCADE 8 MDR USD (2014) DRABBAR 200 000 PATIENTER ÅRLIGEN

BI 505 KAN STIMULERA MAKROFAGER ATT RENSA UPP LÅGA HALTER AV MYELOMCELLER MED MÅL ATT FÖRHINDRA ELLER FÖRDRÖJA ÅTERFALL BEHANDLING AV MUTIPELT MYELOM MED TOXISKA SLEDGEHAMMER LÄKEMEDEL BI-505 STIMULERAR MAKROFAGER ATT ÄTA UPP MYELOMCELLER Cancer Cancer Cancer Cancer -cell Friska celler Cancer -cell Cancer -cell Friska celler Friska celler MAKROFAG Cancer Cancer Cancer Cancer

BI-1206 NON-HODGKINS LYMFOM/KRONISK LYMFATISK LEUKEMI LIVSHOTANDE BLODCANCER ANGREPPSPUNKT: CD32B REDUCERAR RESISTENSPROBLEM POTENTIERAR MARKNADSLEDANDE LÄKEMEDEL HAR EGEN CELLDÖDANDE EFFEKT MOT CANCER FINANSIERING AV OCH SAMARBETE MED CRUK MABTHERA 6,6 MDR USD 2013 (NHL) POTENTIAL ÄVEN INOM ANDRA SEGMENT (TEX CD38) NHL DRABBAR >12 000 PATIENTER ÅRLIGEN START AV FAS I/II H2 2015

TB-403 MEDULLOBLASTOM/NEUROBLASTOM LIVSHOTANDE CANCER SOM DRABBAR BARN ANGREPPSPUNKT: PIGF MÖJLIG BREAKTHROUGH THERAPY DESIGNATION SAMARBETE MED THROMBOGENICS UTMÄRKT SÄKERHETSPROFIL I TIDIGARE KLINISKA PRÖVNINGAR NY KUNSKAP OM VERKNINGS- MEKANISMEN START AV FAS I/II H2 2015

BIOINVENTS PARTNERS 6 4 4 Globala läkemedelsbolag som partners Pågående Fas I-studier Pågående prekliniska studier och ett flertal projekt i discoveryfas 150 Mkr i intäkter 2012-2014

BIOINVENTS PREKLINISKA PROJEKT

REGULATORISKA T-CELLER (T-REGS) SÅ FUNGERAR DET REGULATORISKA T-CELLER CD25 CD4 BIOINVENTS ANTIKROPPAR KROPPENS IMMUNFÖRSVAR - FOXP3 dödar cancerceller motverkar infektioner autoimmuna sjukdomar + + Cancer -cell Cancer -cell Cancer -cell Cancer -cell

ANTIKROPPAR MOT T-REGS KAN BLI NÄSTA STORA GENOMBROTT I BEHANDLING AV CANCER Immunogenic intensification Checkpoint inhibitor alone

BIOINVENTS AFFÄRSMODELL

BIOINVENTS AFFÄRSMODELL F.I.R.S.T. -BioInvents verktyg för att hitta rätt antikropp EGNA LÄKEMEDELSPROJEKT n-coder - BioInvents bibliotek med 20-30 miljarder antikroppar BETALANDE KUNDER F.I.R.S.T. n-coder

FOKUS 2015 KLINISK PROGRESS OCH PARTNERAVTAL F.I.R.S.T. -BioInvents verktyg för att hitta rätt antikropp EGNA LÄKEMEDELSPROJEKT n-coder - BioInvents bibliotek med 20-30 miljarder antikroppar BETALANDE KUNDER F.I.R.S.T. n-coder INTENSIFIERAD MARKNADSFÖRING FORTSATTA INTÄKTER

FINANSIELL ÖVERSIKT Jan-dec Jan-dec MSEK 2014 2013 Nettoomsättning 47 82 FoU -73-71 Försäljning- & administrationskostnader -32-30 -105-101 Övriga rörelseintäkter & kostnader 3,4 0,5 Rörelseresultat -55-19 Finansnetto 0,9 1,1 Resultat efter skatt -54-18 Livkida medel 46 65 24

FULLT GARANTERAD FÖRETRÄDESEMISSION OM CIRKA 75 MSEK Emissionen är säkerställd upp till 100 procent, inkluderande teckningsåtaganden (i vissa fall utöver tidigare pro rata-andel) från välrenommerade life science-investerare såsom Healthcare Equity L/S, Vixco Capital AB/Mats Thorén och East Bay AB (Peter Thelin family office) Management och nyckelpersoner har lämnat teckningsåtaganden Slutliga emissionsvillkor meddelas senast den 17 april 2015 Teckningsperiod mellan 28 april 13 maj 2015 Emissionslikviden stärker BioInvents finansiella ställning och säkerställer kapitalbehov under kommande 12-18 månader 25

SAMMANFATTNING AV NYHETSFLÖDET BI-505 FAS IIA-STUDIE I SAMARBETE MED UNIVERSITY OF PENNSYLVANIA BI-1206 FAS I/II-STUDIE MED FULL FINANSIERING AV CRUK TB-403 FAS I/II-STUDIE I PEDIATRISK CANCER

NEXT GENERATION ANTIBODIES IN IMMUNO ONCOLOGY Björn Frendéus, PhD, CSO Anna Wickenberg, PhD, VP Clinical Development BioInvent International AB Capital market presentation 23 March 2015, Stockholm, Sweden

AGENDA The importance of F.I.R.S.T discovery of antibodies and targets BI-1206 antibody targeting CD32b with significant potential for B cell cancer BI-505 ICAM-1 antibody to overcome MRD in Multiple Myeloma TB-403 antibody targeting the PlGF/Nrp1 pathway in childhood cancer Next generation mab targeting Tregs and TAMs for cancer therapy 29

Tumor cell death (%) THE DYNAMIC BIOLOGY OF ANTIBODIES Type II Type I B1 Rituximab 1F5 Ab mechanism-of-action Programmed cell death In vivo therapeutic activity Complement Cell lysis CDC Three CD20 antibody clones (Rituximab, 1F5, B1) on same backbone (Fc) Similar affinities (Kd = 3-8 nm) Cragg & Glennie 2004 32 Cragg & Glennie

ANTIBODY BIOLOGY DETERMINES CLINICAL EFFICACY Media Release Basel, 24 July 2013 Roche's obinutuzumab (GA101) delayed disease progression longer than MabThera/Rituxan in people with one of the most common forms of blood cancer Phase III CLL11 study showed GA101 plus chlorambucil, a chemotherapy, was superior to MabThera/Rituxan plus chlorambucil in helping people with previously untreated chronic lymphocytic leukemia live longer without their disease worsening About obinutuzumab (GA101) GA101 is the first investigational type II, glycoengineered medicine designed to attack cells that have a certain marker (CD20) on their surface. It attacks targeted cells both directly and together with the body s immune system. GA101 is currently being investigated in a large clinical program, including multiple head-to-head phase III studies versus MabThera/Rituxan in indolent non-hodgkin lymphoma (NHL) and diffuse large B-cell lymphoma (DLBCL). In the U.S., GA101 is being developed and will be commercialized in collaboration with Biogen Idec. 33

F.I.R.S.T TM DISCOVERY FUNCTION, RATHER THAN TARGET, DEFINED Differential cell panning to isolate pools of antibodies Mapping of Ab target specificities scfv/fab Heat map antibody binding to different Cell types (FACS) 10 000 scfv/fab analyzed Identification of unique clones Syngeneic mouse models High throughput IgG production DNA sequencing 500-1000 scfv/fab analyzed In vitro testing (Functionality e.g. ADCC, PCD, internalization) ~500 IgG analyzed Function-first screening Patient materials Target identification Target id. ~100 IgG analyzed In vivo ~10 IgG A function-led discovery platform for combined antibody and target discovery 34

F.I.R.S.T TM GENERATED PROGRAMS Multiple Myeloma (ICAM-1, BI-505) B cell malignancy/lymphoproliferative Diseases (CD32b, BI-1206) Over coming antibody drug resistance Regulatory T cells (discovery stage) Discovery of T-Reg modulating and depletion mabs and targets Tumor associated macrophages (discovery stage) Shifting TAM toward M1 phenotype 35

CLL cells F.I.R.S.T TM ANTI-CLL ANTIBODIES Patient materials Discovery of mab and targets with superior PCD and ADCC activity 1. Differential cell panning TARGET CLL cells from 10 patients + NON-TARGET PBMC +/- B cells 3. Identification of unique clones 550 unique clones identified, yielding ~80 unique binding patterns 2. Screening of scfv Cell binding in flow cytometry; 7000 clones analyzed Flow cytometry mapping of unique scfv against CLL cells, normal B cells and various cancer cell lines PBMC 4. High throughput IgG production 300 clones produced as IgG 36

CLINICALLY RELEVANT TARGETS AND MABS IDENTIFIED Rituximab Patient materials CD200 best-in-class Rituximab ADCC results normalized to Rituximab 37 37

BIOINVENT CANCER & IMMUNOLOGY IN VIVO MODELS 1. In vivo screening models (cell lines) Scid/ARH-77 (sc, iv) Scid/Daudi (sc) Scid/Raji (sc/iv) Scid/Granta (sc, iv) Scid/Jeko (sc/iv) Scid/RPMI-8226 (sc, iv) NOG/U266 (iv) Scid/OPM-2 (sc) Scid/EJM (sc) Balb/c/4T1 (sc, ortho) C57BL/6 ID8 (i.p.) Scid/PC-3 (sc) Scid/DU-145 (sc) Balb/c-4T1 (orthopic) C57BL/6 ID8 (i.p.) Balb/c-CT26 (s.c) C57BL/6 B16.F12 (s.c) C57BL/6 MB49 (s.c) Lymphoma/leukaemia* Mantle Cell Lymphoma* Multiple myeloma* Immune modulation* Solid cancer models 2. Immunomodulation models (M1/M2, TH1/TH2) and Target validation (PoC) 4T1 (Balb/c )* B16-F10 (C57/Bl6)* ID8(C57/Bl6)* KPC, KrasP53 double TG** (Hagemann Lab) Pancreatic Cancer TCL1 TG mice ** (SOTON) Chronic Lymphocytic Leukaemia 3. Identification of therapeutically optimal lead candidate human mab and clinically optimal target/epitope Nod/scid-irrad*. Chronic Lymphocytic Leukaemia (BM/Spleen) Nod/scid-irrad*. Acute Myeloid Leukaemia (BM/Spleen) Nod/scid-irrad*. Mantle Cell Lymphoma (BM/Spleen) Hu-scid.* Multiple myeloma (fully human BM) *or NOD/scid-IL-2rg-/- 4. MoA related models, transgenes & KOs Scid/common g chain -/- (activatory FcgR dependency)** Scid/cd32b-/- (inhibitory FcgR dependency)** Shi-scid-IL-2rg-/- (NK cell deficient)* Clodronate liposome depletion (Macrophage-dependent MoA)* Anti-asialo mab (NK cell dependent MoA)* 42

CD32B ON TARGET B-CELLS REDUCES RITUXIMAB EFFICACY THROUGH INTERNALIZATION Mantle cell lymphoma Follicular lymphoma Lim et. al; Blood. 2011 Lee, Br J Hematol. 2014 45

FCGRIIB DE-SENSITIZES IMMUNE EFFECTOR CELLS AND MUTES ANTI-CANCER MAB THERAPEUTIC ACTIVITY wt g -/- FcgRIIb -/- 47

% internalized CD20 BI-1206 BLOCKS RITUXIMAB INTERNALIZATION Novel mechanism to overcome anti-body drug resistance 90 80 70 60 50 40 30 2h 6h 20 10 0 Rituximab Rituximab + CD32B (1:1) Rituximab Rituximab + CD32B (1:1) Rituximab Rituximab + CD32B (1:1) Pat 1 Pat 2 Pat 3 48

% macrophages loaded with CLL cells BI-1206 ENHANCES RITUXIMAB ADCP THROUGH INHIBITION OF CD20 INTERNALIZATION IN VITRO Anti-CD32b significantly enhances rituximab ADCP in primary CLL 70 60 50 rituximab + isotype control N297Q rituximab + CD32B N297Q *** 40 30 20 *** * 10 0 patient 1 patient 2 patient 3 Exprimental setup: pre-incubation with CD32B-N297Q 3h prior to addition of rituximab and monocyte derived macrophages 49

BI-1206 HAS DIRECT CYTOTOXIC ACTIVITY IN VITRO Anti-CD32b is more effective inducer of ADCC, PCD and ADCP compared with rituximab in primary patient CLL cells ADCC PCD ADCP 50

BI-1206 POTENTIATES RITUXIMAB B CELL DEPLETION IN IMMUNOCOMPETENT HCD32 + HCD20 + MCD32B -/- MICE 51

RITUXIMAB EFFECTIVELY DEPLETES SOLITARY, BUT NOT STROMAL-CELL ASSOCIATED, PATIENT CLL CELLS IN VIVO Patient materials hucll-scid mouse Solitary (peritoneum) mab-treatment (ctrl mab or rituximab 10 mg/kg) Stroma (spleen) 52

THERAPEUTIC ANTI-CD38 AND ANTI-CD19 ANTIBODIES ARE ALSO INTERNALIZED IN A CD32B-DEPENDENT MANNER 53 53

CLINICAL DEVELOPMENT OF BI-1206 56

INSIGHTFUL KOL FEEDBACK ON BI-1206 DATA PACKAGE Unmet Needs in DLBCL Relapse, Refractory and failed HSCT is a pressing unmet need as nothing keeps patients alive longer than 6 months - nnn, MD, Roswell Park Cancer Center Treatment I can t see rituximab going away in the near future, the data I ve seen from Gazyva doesn t support replacing rituximab, plus everybody in the world is familiar with rituximab - US Lymphoma Expert Treatment If you have a mab to overcome rituximab resistance, then you have something great and immediately useful and a big product across all B-Cell malignancies. - US Hem/Onc Expert Unmet Needs in CLL Now obviously if you would take CD-20 therapy and further enhance that with another antibody, I think there would be a lot of enthusiasm for that - nnn, Mayo Clinic 57

14-BI-1206-1: A SIGNAL SEEKING PHASE I/IIA SAFETY STUDY WITH BI- 1206 AND RITUXIMAB IN PATIENTS WITH CD32B+ B CELL MALIGNANCY First In Man 4 sites in UK is planned to participate Coordinating PI Prof Andrew Davies, Southampton 58

14-BI-1206-1: A SIGNAL SEEKING PHASE I/IIA SAFETY STUDY WITH BI- 1206 AND RITUXIMAB IN PATIENTS WITH CD32B+ B CELL MALIGNANCY PART A Establish safety and toxicity profile of BI-1206 Determine the maximal tolerated dose or the dose at which CD32b is completely saturated PART B Establish further safety and tolerability of BI-1206 as a single agent and in combination with rituximab Document anti-tumor activity in patients with relapsed or refractory B-cell malignancies as a single agent or in combination with rituximab Indicate possible and optimal downstream clinical development paths 59

14-BI-1206-1: A SIGNAL SEEKING PHASE I/IIA SAFETY STUDY WITH BI- 1206 AND RITUXIMAB IN PATIENTS WITH CD32B+ B CELL MALIGNANCY A multicenter first in man, open label, two part, phase I/IIa study in patients with relapsed or refractory CD32b positive B cell malignancies. Part A : Part B: Single agent BI-1206 dose escalation, classic 3+3 design Open, randomized, two-armed study to investigate Single agent BI- 1206 at R2PD and Combination of BI-1206 at R2PD and rituximab enriched for CLL & MCL patients (high CD32b expression) 3/24/2015 60

BUILDING EVIDENCE TO SUPPORT DEVELOPMENT OF BI-1206 THROUGH MULTIPLE PATHWAYS Clinical Study 14-BI-1206-001 Preclinical studies - Bio bank sample phenotyping - acd38 combination in vivo Safety and efficacy signal in combination with rituximab Safety and efficacy signal as single agent in CLL and subtypes of NHL CD32b expression on NHL subtypes In vivo efficacy in combination with acd38 Building a body of evidence and data Multiple Ph II options emerging 62 62

MULTIPLE PH II CLINICAL DEVELOPMENT OPPORTUNITIES MAY EMERGE Building a body of evidence and data Multiple Ph II options emerging acd20 Combination with other mabs PhII combo in CLL, MCL and/or NHL relapsed/refractory and/or patients unfit for chemotherpy acd38 PhII combo with in multiple myelom Single agent In relapsed/refractory CLL, MCL and/or NHL BI-1206 effect in combination with tyrosine kinase inhibitors in CLL or MCL in MM; single agent and/or combination effects with current and emerging SoC 63 activity in autoimmune disorders 63

Depth of response MINIMAL RESIDUAL DISEASE SETTING IS OPTIMAL THERAPEUTIC USE FOR BI-505 BASED ON MODE OF ACTION Trial in smoldering MM sledgehammer e.g. MPV, bortesomib, revlimid Phase I patients TTP sledgehammer sledgehammer + BI-505 MRD BI-505 MoA 1. Activates macrophages in BM compartments, which in the absence of BI-505 support MM survival and drug-resistance, to kill off MM cells (TAM reprogramming) 2. Super induces macrophage effector cell influx into Multiple Myeloma bone marrow 3. Blocking of ICAM-1 mediated cell adhesion induced drug resistance 65

THE SLEDGE HAMMER COMBINATION CONCEPT: ENHANCED EFFICACY FOLLOWING COMBINATION OF BI-505 WITH REVLIMID OR BORTEZOMIB AUC, tumor growth Survival The combination of BI-505 and Revlimid or Velcade significantly enhances the therapeutic effect in subcutaneous RPMI-8226 model. Treatments were performed in a therapeutic setting and was started only once well-established tumors (3x3 mm)were formed and were thereafter continued for 150 days. Importantly 4 out of 5 lenalidomide + BI-505 and 2 out of 5 bortezomib + BI-505 treated mice were completely tumor free at termination. Remaining mice were terminated due to high tumor burden. Antibodies were administered i.p. 2 times/week and bortezomib i.v. once/week. Lenalidomide was administered p.o. 5 times/week for two consecutive weeks followed by one week of washout and thereafter repeated. Treatment stopped at day 150. N=5-6 mice / group *=p<0,05, ** = p<0,01 73

MECHANISM OF ACTION: BI-505 HAS MACROPHAGE DEPENDENT IN VIVO ANTI-MYELOMA ACTIVITY Figure 6. BI-505 confers Fc-FcgR dependent antitumor activity through macrophages Veitonmäki et al, Cancer Cell, 2013 E) Tumor growth in macrophage or NK cell depleted SCID mice bearing established RPMI-8226 myeloma tumors treated with BI-505 or control antibody. ***p < 0.001. G) Tumor growth in BI-505 or control antibody treated NK-cell deficient NOD/Shi-scid/IL-2Rg -/- mice transplanted with RPMI- 8226 myeloma cells. ***p < 0.001. 76

MECHANISM-OF-ACTION: BI-505 INDUCES MACROPHAGE INFILTRATION TO TUMOR LESIONS BI-505 causes a significant influx of macrophages in tumors compared to isotype control treated mice (upper panel and diagram), suggesting that macrophages are the dominant effector cells 77

Mechanism-of-action MACROPHAGES AND ICAM-1 ARE IMPLICATED IN MM DRUG RESISTANCE 80

CLINICAL DEVELOPMENT OF BI-505 MULTIPLE MYELOMA 81

BI-505 CLINICAL PHASE I DOSE ESCALATING STUDY - CONCLUSIONS BI-505 has a favorable safety profile in doses up to 20 mg/kg 2qw At dosing 10 mg/kg, exposure levels needed for complete receptor saturation on bone marrow MM cells was achieved Of the 29 treated patients in dose group 6 and onwards (dose 0.09 20 mg/kg), 7 patients, 24 % had stable disease for at least 2 months. 16/29 patients were treated with doses below receptor saturation level Response data is comparable to elotuzumab (acs1) phase I single agent therapy data

INSIGHTFUL KOL FEEDBACK ON BI-505 DATA PACKAGE Unmet Need Basically resistance is the biggest concern, in reality we have only two classes of drugs, therefore agents that can deepen a response that could play a meaningful role in delaying the time to relapse -nnn, MD -Dana Farber Unmet Need Treatments that have a lower toxicity for patients, as most are elderly and on the treatments for prolonged periods of time, or increases in PFS. Ideally treatments that can provide both low toxicity and longer PFS -nnn, MD - Duke Method of Action If BI-505 can clean up MRD that other treatments miss, then you ve got something really compelling -nnn, MD -University of Pennsylvania Phase I Data given that it is a heavily treated population, I wouldn t readily dismiss the 25% stable disease you observed in your earlier trial. -nnn, MD/PhD - MD Anderson 83

URGENT MEDICAL NEED IN MM PATIENTS Relapse Patients relapse and become resistant to available therapies Side effects Limited options Need Increased burden of disease and cumulative side effects with each new treatment line elderly patients - balance between tumor control and managing side effects Treatment currently include 2 major classes: Proteasome inhibitors (bortezomib, carfilzomib) imid (lenalidomide, thalidomide, pomalidomid) Urgent need for treatments with new mechanisms of action Significant interest in new agents with low toxicity to deepen response by targeting MRD 84

Depth of response MINIMAL RESIDUAL DISEASE SETTING IS OPTIMAL THERAPEUTIC USE FOR BI-505 BASED ON MODE OF ACTION Trial in smoldering MM sledgehammer e.g. MPV, bortesomib, revlimid Phase I patients TTP sledgehammer sledgehammer + BI-505 MRD BI-505 MoA 1. Activates macrophages in BM compartments, which in the absence of BI-505 support MM survival and drug-resistance, to kill off MM cells (TAM reprogramming) 2. Super induces macrophage effector cell influx into Multiple Myeloma bone marrow 3. Blocking of ICAM-1 mediated cell adhesion induced drug resistance 86

MULTIPLE MYELOMA ROLE FOR MONOCLONAL ANTIBODIES Remitting and relapsing disease - ultimately incurable Evidence for minimal residual disease negativity predicting for PFS and OS Aim to deepen and prolong responses in combination with existing agents SLAMF7 (CS1), elotuzumab Phase I/II monotherapy best response stable disease 26.5% comparable to BI-505 ph I Phase I combination with lenalidomide and dexamethasone 82% PR Phase III trials ongoing ; CD38, eg daratumumab Phase I monotherapy 42% PR Phase II combination with lenalidomide and dexamethasone 86% PR Phase III trials ongoing Deep responses but duration unclear

BI-505 POST AUTOLOGOUS STEM CELL TRANSPLANTATION PHASE II SIGNAL SEEKING CLINICAL STUDY PLANNED investigate safety and efficacy of BI-505 in combination with maintenance lenalidomide in multiple myeloma patients post autologous stem-cell transplantation (ASCT) low tumor burden, but patients relapse eventually investigating if BI-505 has the potential to deepen the response post ASCT One-armed open study, a matching historical control cohort treated with lenalidomide will be selected from a similar protocol ASCT N 30, treated with BI-505 and lenalidomide for 9 mo, 1 y post-asct Readout: safety proportion of patients in CR MRD Macrophage PD markers 89

F.I.R.S.T. - REGULATORY T CELLS BioInvent has unique knowledge and access to; Regulatory T cells including protocols to generate these cells(target cells) Normal cytotoxic (and helper) T cells (non-target cells) High-throughput in vitro functional assays for assessment of antibody depleting activity against regulatory T cells (targets) and cytotoxic T cells (non-targets) Immunocompetent in vivo models for proof-of-concept studies Strong knowledge and experience from working with T cell and immune cell based immunological assays for assessment of efficacy and safety (at regulatory level) There is great potential for immune modulatory antibodies Huge market and great commercial potential for more active single or combination antibody therapies, showing increased efficacy but also improved safety, in larger patient populations F.I.R.S.T platform ideally suited to identify optimal targets and antibodies with superior specificity and depleting activity, against regulatory T cells 110

F.I.R.S.T TAM Tumor Associated Macrophages (TAM s) are pro-tumorigenic, enhance tumor growth and progression, and decrease efficacy of various anticancer therapies. Macrophages are, however, plastic and can be re-educated. The aim is to generate immunomodulatory antibodies targeting TAMs for therapy of cancer. Anti-TAM antibodies may act by several mechanisms-of-action to relieve immune suppression and enhance antitumor activity: Deplete, re-educate and/or block recruitment of TAM Improve innate (MF) and adaptive (CD8 T cell) antitumor immunity Aim: Using the n-coder F.I.R.S.T platform and primary myeloid cells isolated from tumors of M2/TH2- prone, as well as M1/TH1 prone mice, a diverse pool of antibodies against clinically relevant targets will be identified. Anti-tumor 1.Pro-inflammatory 2.Activate anti-tumor immunity 3.Direct tumoricidal effects M1 M2 (includes TAMs) Pro-tumor 1. Suppress anti-tumor immunity 2. Pro-angiogenic 3. Production of tumor growth factors 4. Facilitate metastasis 111

- SYNERGY BETWEEN TARGETING T REG AND TAM -Tumor lysis -Antigen release -Inflammation 1 3 + APC (DC or MF) TAM - + + + + CD4 + T h cell - - CD8 + T cell Tumor cell death T reg cell -APC activation -Cytokine production - 2 APC + + CD8 + T cell activation + CD4 + TAM + - CD8 + Cytotoxic T cell + 112