BioInvent International AB · OMXSTO:BINV
BioInvent International AB — Investor Day (March 2015)
70 slides from BioInvent International AB's investor day presentation, Mar 23, 2015
Slide 1: Kapitalmarknadspresentation 23 mars 2015
KAPITALMARKNADSPRESENTATION 23 MARS 2015 MICHAEL OREDSSON, VD
Slide 2: Stabil bas och betydande uppsida
STABIL BAS OCH BETYDANDE UPPSIDA Bioinvent… …har fokus på …har en immunonkologi och …har tre produkter på väg teknologiplattform som erbjuder signifikant in i klinisk fas I/II redan skapat stort värde mervärde för patienter och partners ↪ från prekliniskt till kliniskt bolag under 2015 ↪ kraftig häv
Slide 3: Affärsstrategi
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 proje
Slide 4: Agenda
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
Slide 5: Immunonkologi – framtidens behandling av cancer
IMMUNONKOLOGI – FRAMTIDENS BEHANDLING AV CANCER ASCO 78 CHICAGO KLINISKA >1 MILJARD USD MAJ 2014 PRÖVNINGAR (YERVOY) 5
Slide 6: Antikroppsläkemedel hjälper immunförsvaret att döda cancerceller
ANTIKROPPSLÄKEMEDEL HJÄLPER IMMUNFÖRSVARET ATT DÖDA CANCERCELLER YER VOY Immunsystemet är Monoklonala Immuno-onkologiska Antikroppsläkemedel kroppens mest kraftfulla antikroppar fäster på antikroppsläkemedel har dubbelt så hög och effektiva verktyg för målceller och hjälper har redan nått chans att
Slide 7: Behandling av cancer
BEHANDLING AV CANCER UNDERSTÖDJANDE KIRURGI STRÅLBEHANDLING CELLGIFTER IMMUNONKOLOGI BEHANDLING
Slide 8: Bioinvents verktyg för nya cancerterapier
BIOINVENTS VERKTYG FÖR NYA CANCERTERAPIER
Slide 9: BioInvent hittar rätt antikroppar
BIOINVENT HITTAR RÄTT ANTIKROPPAR F.I.R.S.T.™ Agnas med celler från patienter –BioInvents verktyg för att hitta rätt antikropp n-CoDeR® - BioInvents bibliotek med 20-30 miljarder antikroppar
Slide 10: F.I.R.S.T – Bioinvents unika metod att hitta rätt antikropp
F.I.R.S.T® – BIOINVENTS UNIKA METOD ATT HITTA RÄTT ANTIKROPP friska celler sjuka celler 1. Antikropps- 2. Vi identifierar de 3. Dessa 4. De bästa 5. Dessa anti- biblioteket screenas antikroppar som antikroppar testas antikropparna väljs kroppar testas mot sjuka och friska binder till sjuka in vitro
Slide 11: 2015 – ett transformerande år, tre produkter i klinisk fas I/II
2015 – ETT TRANSFORMERANDE ÅR TRE PRODUKTER I KLINISK FAS I/II
Slide 12: Bioinvent fokuserar på cancer
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
Slide 13: BI-505 – Multipelt myelom
BI-505 – MULTIPELT MYELOM LIVSHOTANDE BLODCANCER MED UPPREPADE ÅTERFALL REVLIMID/VELCADE ANGREPPSPUNKT: ICAM-1 SOM PÅVERKAR 8 MDR IMMUNSYSTEMETS USD MAKROFAGER (2014) SYNERGI MED REVLIMID/VELCADE DRABBAR GOD SÄKERHET OCH DJUP RESPONS KAN 200 000 HINDRA/FÖRDRÖJA PATIENTER ÅTERFALL ÅRLIGEN START AV FA
Slide 14: BI-505 kan stimulera makrofager att rensa upp låga halter av myelomceller
BI–505 KAN STIMULERA MAKROFAGER ATT RENSA UPP LÅGA HALTER AV MYELOMCELLER MED MÅL ATT FÖRHINDRA ELLER FÖRDRÖJA ÅTERFALL BEHANDLING AV MUTIPELT MYELOM MED BI-505 STIMULERAR MAKROFAGER TOXISKA ”SLEDGEHAMMER” LÄKEMEDEL ATT ”ÄTA UPP” MYELOMCELLER Cancer Cancer Cancer Cancer Cancer Cancer -cell -cell Fri
Slide 15: BI-1206 – Non-Hodgkins lymfom/kronisk lymfatisk leukemi
BI-1206 – NON-HODGKINS LYMFOM/KRONISK LYMFATISK LEUKEMI LIVSHOTANDE BLODCANCER MABTHERA ANGREPPSPUNKT: 6,6 MDR CD32B USD 2013 (NHL) • REDUCERAR POTENTIAL ÄVEN INOM RESISTENSPROBLEM ANDRA SEGMENT • POTENTIERAR (TEX CD38) MARKNADSLEDANDE LÄKEMEDEL • HAR EGEN CELLDÖDANDE NHL DRABBAR EFFEKT MOT CANCER >
Slide 16: TB-403 – Medulloblastom/Neuroblastom
TB-403 – MEDULLOBLASTOM/NEUROBLASTOM LIVSHOTANDE CANCER SOM DRABBAR BARN UTMÄRKT SÄKERHETSPROFIL ANGREPPSPUNKT: I TIDIGARE PIGF KLINISKA PRÖVNINGAR MÖJLIG BREAKTHROUGH THERAPY DESIGNATION NY KUNSKAP OM SAMARBETE MED VERKNINGS- THROMBOGENICS MEKANISMEN START AV FAS I/II H2 2015
Slide 17: Bioinvents partners
BIOINVENTS PARTNERS 6 Globala läkemedelsbolag 4 4 Pågående Fas I-studier Pågående prekliniska studier som partners …och ett flertal projekt i discovery- fas 150 Mkr i intäkter 2012-2014
Slide 18: Bioinvents prekliniska projekt
BIOINVENTS PREKLINISKA PROJEKT
Slide 19: Regulatoriska T-celler (T-regs) – så fungerar det
REGULATORISKA T-CELLER (T-REGS) – SÅ FUNGERAR DET REGULATORISKA T-CELLER CD4 BIOINVENTS CD25 ANTIKROPPAR - FOXP3 KROPPENS IMMUNFÖRSVAR dödar cancerceller autoimmuna motverkar infektioner sjukdomar + + Cancer Cancer -cell -cell Cancer -cell Cancer -cell
Slide 20: Antikroppar mot T-regs kan bli nästa stora genombrott i behandling av cancer
ANTIKROPPAR MOT T-REGS KAN BLI NÄSTA STORA GENOMBROTT I BEHANDLING AV CANCER Immunogenic intensification Checkpoint inhibitor alone
Slide 21: Bioinvents affärsmodell
f = 7 to Q oO = YN & re L <— YN - z Lo a = Oo co |
Slide 22: Bioinvents affärsmodell
BIOINVENTS AFFÄRSMODELL F.I.R.S.T.™ EGNA -BioInvents verktyg för LÄKEMEDELSPROJEKT att hitta rätt antikropp BETALANDE KUNDER n-CoDeR® - BioInvents bibliotek med 20 - 30 miljarder F.I.R.S.T. ™ antikroppar n-CoDeR®
Slide 23: Fokus 2015
FOKUS 2015 KLINISK PROGRESS OCH PARTNERAVTAL F.I.R.S.T.™ EGNA -BioInvents verktyg för LÄKEMEDELSPROJEKT att hitta rätt antikropp BETALANDE KUNDER n-CoDeR® - BioInvents bibliotek med 20 - 30 miljarder F.I.R.S.T. ™ antikroppar n-CoDeR® INTENSIFIERAD FORTSATTA MARKNADSFÖRING INTÄKTER
Slide 24: Finansiell översikt
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
Slide 25: Fullt garanterad företrädesemission om cirka 75 MSEK
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
Slide 26: Sammanfattning av nyhetsflödet
SAMMANFATTNING AV NYHETSFLÖDET BI-1206 BI-505 FAS I/II-STUDIE MED FULL FAS IIA-STUDIE I FINANSIERING AV SAMARBETE MED CRUK UNIVERSITY OF PENNSYLVANIA TB-403 FAS I/II-STUDIE I PEDIATRISK CANCER
Slide 27: Tack
TACK
Slide 28: Next generation antibodies in immuno oncology
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
Slide 29: Agenda
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 mA
Slide 30: The dynamic biology of antibodies
THE DYNAMIC BIOLOGY OF ANTIBODIES Type II Type I Ab mechanism-of-action B1 Rituximab 1F5 Programmed cell death Tumor cell death (%) In vivo therapeutic activity Complement Cell lysis CDC •Three CD20 antibody clones (Rituximab, 1F5, B1) on same backbone (Fc) Cragg & Glennie Cragg & Glennie 2004 •Simi
Slide 31: Antibody biology determines clinical efficacy
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
Slide 32: F.I.R.S.T discovery
F.I.R.S.TTM 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 DNA sequencing
Slide 33: F.I.R.S.T generated programs
F.I.R.S.TTM 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 (discov
Slide 34: F.I.R.S.T anti-CLL antibodies
F.I.R.S.TTM ANTI-CLL ANTIBODIES Patient materials Discovery of mAb and targets with superior PCD and ADCC activity 1. Differential cell panning 3. Identification of unique clones 550 unique clones identified, yielding ~80 unique binding patterns TARGET NON-TARGET CLL cells from + PBMC +/- B cells 10
Slide 35: Clinically relevant targets and mAbs identified
CLINICALLY RELEVANT TARGETS AND MABS IDENTIFIED Patient materials Rituximab CD200 ”best-in-class” Rituximab ADCC results normalized to Rituximab 37 37
Slide 36: BioInvent cancer & immunology in vivo models
BIOINVENT CANCER & IMMUNOLOGY IN VIVO MODELS 1. In vivo screening models (cell lines) 2. Immunomodulation models (M1/M2, TH1/TH2) Scid/ARH-77 (sc, iv) and Target validation (PoC) Scid/Daudi (sc) Lymphoma/leukaemia* 4T1 (Balb/c )* Scid/Raji (sc/iv) B16-F10 (C57/Bl6)* ID8(C57/Bl6)* Scid/Granta (sc, iv
Slide 37: Agenda
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 mA
Slide 38: CD32B on target B-cells reduces rituximab efficacy through internalization
CD32B ON TARGET B-CELLS REDUCES RITUXIMAB EFFICACY THROUGH INTERNALIZATION Lim et. al; Blood. 2011 Lee, Br J Hematol. 2014 Mantle cell lymphoma Follicular lymphoma 45
Slide 39: FcgRIIB de-sensitizes immune effector cells and mutes anti-cancer mAb activity
FCGRIIB DE-SENSITIZES IMMUNE EFFECTOR CELLS AND MUTES ANTI-CANCER MAB THERAPEUTIC ACTIVITY wt g -/- FcgRIIb -/- 47
Slide 40: BI-1206 blocks rituximab internalization
BI-1206 BLOCKS RITUXIMAB INTERNALIZATION Novel mechanism to overcome anti-body drug resistance 90 80 70 60 % internalized CD20 50 40 2h 6h 30 20 10 0 Rituximab Rituximab + Rituximab Rituximab + Rituximab Rituximab + CD32B (1:1) CD32B (1:1) CD32B (1:1) Pat 1 Pat 2 Pat 3 48
Slide 41: BI-1206 enhances rituximab ADCP through inhibition of CD20 internalization
BI-1206 ENHANCES RITUXIMAB ADCP THROUGH INHIBITION OF CD20 INTERNALIZATION IN VITRO Anti-CD32b significantly enhances rituximab ADCP in primary CLL 70 rituximab + isotype control % macrophages loaded with CLL cells 60 N297Q *** rituximab + CD32B N297Q 50 40 30 *** * 20 10 0 patient 1 patient 2 patie
Slide 42: BI-1206 has direct cytotoxic activity in vitro
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
Slide 43: BI-1206 potentiates rituximab B cell depletion in immunocompetent mice
BI-1206 POTENTIATES RITUXIMAB B CELL DEPLETION IN IMMUNOCOMPETENT HCD32+HCD20+MCD32B-/- MICE 51
Slide 44: Rituximab depletes solitary, but not stromal-cell associated, CLL cells in vivo
RITUXIMAB EFFECTIVELY DEPLETES SOLITARY, BUT NOT STROMAL-CELL ASSOCIATED, PATIENT CLL CELLS IN VIVO Patient materials huCLL-scid mouse mAb-treatment (ctrl mAb or rituximab 10 mg/kg) Solitary (peritoneum) Stroma (spleen) 52
Slide 45: Anti-CD38 and anti-CD19 antibodies also internalized in CD32B-dependent manner
THERAPEUTIC ANTI-CD38 AND ANTI-CD19 ANTIBODIES ARE ALSO INTERNALIZED IN A CD32B-DEPENDENT MANNER 53 53
Slide 46: Clinical development of BI-1206
CLINICAL DEVELOPMENT OF BI-1206 56
Slide 47: Insightful KOL feedback on BI-1206 data package
INSIGHTFUL KOL FEEDBACK ON BI-1206 DATA PACKAGE Unmet Needs in DLBCL Treatment “Relapse, Refractory and failed HSCT is a “I can’t see rituximab going away in the near future, pressing unmet need as nothing keeps the data I’ve seen from Gazyva doesn’t support patients alive longer than 6 months” repl
Slide 48: 14-BI-1206-1: Phase I/IIa safety study with BI-1206 and rituximab
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
Slide 49: 14-BI-1206-1: Phase I/IIa study objectives, Part A and B
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 PART B • Establish safety and toxicity profile of • Establish further safety and BI-1206 tolerability of BI-1206 as a single • Determine the maximal tolerated agent an
Slide 50: 14-BI-1206-1: Phase I/IIa study design
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 : • Single agent BI
Slide 51: Building evidence to support development of BI-1206 through multiple pathways
BUILDING EVIDENCE TO SUPPORT DEVELOPMENT OF BI-1206 THROUGH MULTIPLE PATHWAYS Clinical Study Preclinical studies - Bio bank sample phenotyping 14-BI-1206-001 - aCD38 combination in vivo Safety and efficacy Safety and efficacy In vivo efficacy in signal in signal as single CD32b expression combinatio
Slide 52: Multiple Ph II clinical development opportunities may emerge
MULTIPLE PH II CLINICAL DEVELOPMENT OPPORTUNITIES MAY EMERGE Building a body of evidence and data Multiple Ph II options emerging Combination with Single agent other mAbs aCD20 In relapsed/refractory CLL, MCL and/or NHL PhII combo in CLL, MCL and/or NHL relapsed/refractory and/or patients unfit for
Slide 53: Agenda
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 mA
Slide 54: Minimal residual disease setting is optimal therapeutic use for BI-505
MINIMAL RESIDUAL DISEASE SETTING IS OPTIMAL THERAPEUTIC USE FOR BI-505 BASED ON MODE OF ACTION TTP Trial in smoldering Phase I patients of response MM “sledgehammer” Depth e.g. MPV, bortesomib, revlimid sledgehammer sledgehammer + BI-505 MRD BI-505 MoA 1. Activates macrophages in BM compartments, wh
Slide 55: The sledge hammer combination concept: BI-505 with Revlimid or bortezomib
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
Slide 56: Mechanism of action: BI-505 has macrophage dependent anti-myeloma activity
MECHANISM OF ACTION: BI-505 HAS MACROPHAGE DEPENDENT IN VIVO ANTI-MYELOMA ACTIVITY E) Tumor growth in macrophage or NK cell depleted SCID mice bearing established RPMI-8226 myeloma tumors treated with Figure 6. BI-505 confers Fc-FcgR dependent BI-505 or control antibody. ***p < 0.001. antitumor acti
Slide 57: Mechanism-of-action: BI-505 induces macrophage infiltration to tumor lesions
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
Slide 58: Macrophages and ICAM-1 are implicated in MM drug resistance
Mechanism-of-action MACROPHAGES AND ICAM-1 ARE IMPLICATED IN MM DRUG RESISTANCE 80
Slide 59: Clinical development of BI-505
CLINICAL DEVELOPMENT OF BI-505 MULTIPLE MYELOMA 81
Slide 60: BI-505 clinical phase I dose escalating study - conclusions
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
Slide 61: Insightful KOL feedback on BI-505 data package
INSIGHTFUL KOL FEEDBACK ON BI-505 DATA PACKAGE Unmet Need “Basically resistance is the biggest concern, in Unmet Need reality we have only two classes of drugs, “Treatments that have a lower toxicity for therefore agents that can deepen a response patients, as most are elderly and on the that could
Slide 62: Urgent medical need in MM patients
URGENT MEDICAL NEED IN MM PATIENTS • Patients relapse and become resistant to available therapies Relapse • Increased burden of disease and cumulative side effects with each Side new treatment line – elderly patients - balance between tumor effects control and managing side effects • Treatment curre
Slide 63: Minimal residual disease setting is optimal therapeutic use for BI-505
MINIMAL RESIDUAL DISEASE SETTING IS OPTIMAL THERAPEUTIC USE FOR BI-505 BASED ON MODE OF ACTION TTP Trial in smoldering Phase I patients of response MM “sledgehammer” Depth e.g. MPV, bortesomib, revlimid sledgehammer sledgehammer + BI-505 MRD BI-505 MoA 1. Activates macrophages in BM compartments, wh
Slide 64: Multiple myeloma – role for monoclonal antibodies
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 ; CD38, eg daratumumab • Phase I monothera
Slide 65: BI-505 post ASCT – Phase II signal seeking clinical study planned
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 re
Slide 66: Agenda
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 mA
Slide 67: F.I.R.S.T.™ - Regulatory T cells
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
Slide 68: F.I.R.S.T™ TAM
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 th
Slide 69: Synergy between targeting T reg and TAM
SYNERGY BETWEEN TARGETING T REG AND TAM -APC activation -Cytokine production + + 1 - CD4+ TAM APC - - Th cell 2 + +- (DC or MF) -Tumor lysis -Antigen release -Inflammation + + - APC CD8+ T reg Cytotoxic T cell cell + TAM + - + 3 CD4+ + CD8+ T cell CD8+ T cell Tumor cell death activation 112
Slide 70: Tack
TACK