AbCellera Results Presentation Deck

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#1COPYRIGHT © ABCELLERA Q1 2023 BUSINESS UPDATE MAY 4, 2023 AbCellera#2Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 2 DISCLAIMER This presentation contains forward-looking statements, including statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. The forward-looking statements are based on management's beliefs and assumptions and on information currently available to management. All statements contained in this presentation other than statements of historical fact are forward-looking statements, including statements regarding our ability to develop, commercialize and achieve market acceptance of our current and planned products and services, our research and development efforts, and other matters regarding our business strategies, use of capital, results of operations and financial position, and plans and objectives for future operations. In some cases, you can identify forward-looking statements by the words "may," "will," "could," "would," "should," "expect," "intend," "plan," "anticipate," "believe," "estimate," "predict," "project," "potential," "continue," "ongoing" or the negative of these terms or other comparable terminology, although not all forward-looking statements contain these words. These statements involve risks, uncertainties and other factors that may cause actual results, levels of activity, performance, or achievements to be materially different from the information expressed or implied by these forward-looking statements. These risks, uncertainties and other factors are described under "Risk Factors," "Management's Discussion and Analysis of Financial Condition and Results of Operations" and elsewhere in the documents we file with the Securities and Exchange Commission from time to time. We caution you that forward-looking statements are based on a combination of facts and factors currently known by us and our projections of the future, about which we cannot be certain. As a result, the forward-looking statements may not prove to be accurate. The forward-looking statements in this presentation represent our views as of the date hereof. We undertake no obligation to update any forward-looking statements for any reason, except as required by law.#3Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA M ART Q1 2023. BUSINESS UPDATE SUMMARY. BUILDING THE INDUSTRY'S ENGINE FOR ANTIBODY THERAPEUTICS IN $821M 177 101 P AbCellera 9 in total cash, cash equivalents & marketable securities cumulative programs under contract cumulative partnered programs started molecules in the clinic#4Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 4 All programs leverage partnerships. PARTNER-INITIATED PROGRAMS Discovery Programs Co-Development Programs TECHNOLOGY DEVELOPMENT Pre-Partnered Programs#5Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 5 TECHNOLOGY DEVELOPMENT. T-Cell Engager Platform Solving key challenges in developing T-cell engager cells and specific immune cells called T cells. TCEs T-cell engagers (TCEs) are antibodies with 2 arms that are designed to bind to cancer cancer treatments. work by bringing T cells and cancer cells together and stimulating the T cells to kill the cancer cells. controlling how T cells are activated For the arm that binds to the T cell, the goal is to balance potency & cytokine release. only targeting cancer cells For the arm that binds to the cancer cell, the goal is to target only cancer cells, and not healthy cells.#6Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 6 TECHNOLOGY DEVELOPMENT. T-Cell Engager Platform Create T-cell engagers with optimal properties, fast. AbCellera THE PROBLEM Most T-cell engagers are built from sub-optimal CD3-binders CD3 I-onangages have the potential to be powerful conser treatments, but the small number of available bodies and limited multispecific anging techninkages have been tr 003-binding dovelopmors. Approximately of 1-sell engage in cinical trials an ornered with CD3-binding antibodies derived from 934-2, moustibody discovered in 1985 that is an unstrotrod Encar optopo on the N-tominus of CD3² 334-2 and the CD3-bindshx OK13 and LOTI are often heavily onginoord te moduse the rek of cytokine rolyndrome and to improve developability properti THE GOAL Build optimal T-cell engagers from novel CD3-binding antibodies Identifying-lengejers the balancu unti-tumarponcy with ples, such a cycki syndremo, requires simultaneous tuning of both the CD3 and tumor-binding arms. Pairs of antibodies that co this balansoare ram amotinga need for diverse and developable ontbodies that can be combined and tested city optimal dinio candidat To suaming Tallussapor dovolocmon wo discovered and characted novel C133-binding and with binding and functional proportos that are distings from commonly 3-4-2 To validato our CD3-binding ontbodios, wo ased our baccagneering platform, OrthoMab, to get proof-at-connes 1-el garretting the EGR an PEMA We then orgured tumor coll killing and yun resproflex in benchmark-duived alculus a difforon tumor collinos THE OUTCOME T-cell engagers with high potency and low cytokine release Wo used our high-throughput Teoll osagarplatform in chanseri ho mauting bispaanbodian The results demonst that: Tool engagers enginoored fom AbColon's portfolio da cua-binding funcional pressuperior to bo kmalculac OrthoMabanginsemd 1-aallangage favorable developability and PK properties The opamal CD3-binder depends on several tootom including tumor target ond carpet doty Together, these studies ilustrate that combining novel CD3-binding antibodies, clinically validated muticacific engineering technologies, and an integrated discovery and development in streamlines identification of optimal T-cell engagors for diverse tumor targets. Identifying T-cell engagers with optimal potency & cytokine release profiles with differentiated and developable CD3-binding antibodies T-cell engagers with optimal functional properties We generated proof-of-concept T-cell engagers with high potency and low cytokine release. Tn to sinist Maman ng T We identified T-cell engagers with optimal functional profiles. ABCallera CDS-1 CO Figure 1. T-cell engagere enginoored using diverse CD3-binding antibodies have broad tumor coll killing and cytokine release profiles. Wo generated bitcoin with a fund ifli binding sem (mama) and varied Cli-binding armas Colors discovame or Surat-darved usy our 10 cele mai nema of the cambodies Potency EC) is the concentration al ach trapecie antibody needed to incluces 50% at the masmal I calkmadiate ding of Hela col GOOD M 2. Funct Agrand C3-binting in ACCO3-2 al properties of all angagars engineered w TELAN sydd Dam LALA OrthoMab™ ongineered bispocifics with favorable developability properties. -association Polypty EMELISA SP34-CD3 hindist anodien malacuise Rambodies ongorod using a food EGFR-binding um matarunab) and 3-2) or posatuzumab (SP34-derived) using the assay described in Figum 1 2500 Figura 3. Most OrthoMabangineered bispecifics have developability properties comparable to parental antibodies. The fractional porcentage of carroty pairod vs. incorrectly pairod bispocifics was measured by intoot masa sonotremory (MS). Stability, monomariain self-association, and polyapacity were maand by 09, SEC, AC-SINS. and BVP-ELISA, respectively. CD3 T-cell engager ThCNEER-Omakam Isla 152: (0X3-1 am - Figure 4. An amplary CD3x EQFR bispecific antibody with favorable PK properties. Following a single me/kedonsin 1632 mico (humon felln tragic,), concuntrations were quantified using an electrochemluminosoene Custom-built for different tumor targets We identified optimal CD3-binding arms for different tumor targets. Toallangagar function across different timor targets and target densition Tumor target 0 3 OPE S S S S and D From novel CD3-binding antibodies Fully human CD3-binding antibodies that are distinct from commonly used molecules. Antibay querce diversity overed with aptope data AUTRES humbiasn{Meant Mar Rurca Caltent Antiry Dawnerkith frame Kang OFW Wa Valentine de Puyroiment. Lauren Cord & Che Hans Peter, super me Setaco, Pind Man Courtorial P Char, Chin, Steve Rath, AmyCH A G SK Man, Sun, Aanan Ya Rush Da Tim M, fu Tundan, Bryan C. Darhart antar NOTHERS AFFILIATION Vo La Figure 7. High-throughpat accocement of binding properties realed diverse binding Kinetics and specificities. (A) Binding affinity 10 human 3 ry and no subunts we assum by SP-coupl B E 89 Novel CD3-binding antibodies with diverse binding properties Amage of on and off retse a co Grondbindinga ✔ Leve (3) On and offered by SP- kiros and are plotted along the X and Yaxos with afinitios displayed diagonally CETATS- Figure 5. The optimal CD3-binding arm in dependent on tumor target and target donaity We compared this functions prates of CD3x PSMA and CDS EQFHI-ollungators across ondineemt ning G03-binong arms from AbCall's purel (CD3-4, CD3-2, 003-3) posetustnimah, and other aftond IGF-binding ammatumab) uraft PSMAm (TNB-685) Fusalonal properties for C03 EGFR deserved in Fein Tumoreaking and aytokin mies for CD PSMA bispawam measured 18 hours and 72 sours forlowing addition of the bespecto antibodies for N and 221 til LIVE PORTER ONO # 1886 Figur B. Proprietary immunization protocols ucing humanizedmios yielded CD3-binding antibodies with diverse sequences that bind different upitapes. Anibody were divanity wwwsusing our propranary data visualination aftwars. Colum. Cutr representeres bust on V g and and Moram sonu und CDR longths. The plati colored using data from high-throughput surface plasmonanco (SPR) pilapo binning demosting that the majority of car CD3-binding and bodies bind opitupes that an distinct from all SP34-2. C TOX (C) Subur city works by high-throughput SPH and speed specificity was measured by binding to CHO celk asing other humanoryne CO2. KEY HIGHLIGHTS Fine-tune tumor cell killing and cytokine release using TCEs that are superior to commonly-used molecules#7Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 7 TECHNOLOGY DEVELOPMENT. T-Cell Engager Platform Unlock high-value, difficult cancer targets. THE OPPORTUNITY AbCellera Unlock intracellular tumor targets immunotherapies are transforming cancer treatment by moting the immune system to right cancer. T-cat engagers-a type of immunotherapy-etminste cancer ces by simultaneously binding tumor targets and the T-cell acting protein CD3. Because T-cell engagers cannot socess intracellular targets, their use is limited to targets expressed on the tumor cell surface. Toel engages against peptides oisplayed on major ristocompaticity complexes (MHCS) are proming approach for unlocking previously inaccessible, high-valce. intracellular tumor targets, One such target is metanema associated antigen 4 PMHC (MAGE-44-0MHC), a tumor-specinc antigen expressed by many did tumors, but not by most healthy. THE CHALLENGE Finding rare antibodies against pMHCS MAGE-44-MHCs are challenging immunotherapy targets because (a) proteins within the MAGE-A family are highly homologoue (MAGE A4 is often mutated in tumor cells and there is very low expression of MAGEM OMHO on tumor Antibodies that bind to MAGE-44-MHC with the specificity ond affinity needed to minimize the risk of off-target binding are rare. Those that do bind and have favorable developably profiles are even more rare, making them acut to identity using traditional approaches Furthermore, Toll engager development requires tumor-binding antibodies that function assispecies, creating a need for diverse antibodies that can be paired with CDS-binders and tested for optimal function THE SOLUTION Start with diverse panels of pMHC-binding antibodies. We used our and body discovery and development engine to discover and one MAGE 44 binding antibodies with favorable binding and developablity profes terite huNG L LeadMAGE-AS-RHC arbodies will be selected and paired with our panel of previously described CDS-binding antibodies using our sispecific engineering platform. THE OUTCOME OrthoMa", to streamline the development of MAGE A4 MHC Telenders. We identified a panel of antibodies against MAGE-A4-pMHC with: ☐ diverse sequence and binding profes t-specific, high-offinity binding favorable developability profes Breaking barriers to access intracellular targets with T-cell engagers Discovery of diverse, developable, and ultra-specific antibodies against a MAGE-A4 pMHC 45 diverse antibodies against a MAGE-A4 peptide-MHC target Antody discovery 1.5M se Single-cell screening Mbada acaring any k 466 200 45 de Figure 1. Propriotary immunication technologies and high-throughput semning strategis used to writy and captum wahedy diversity (A) Hum were immuned with human phAGE-A presered on MHC-HLA02-01) (Bu baad-besed single-oal soaring assays were used to sees 1.5 milion single Bells and identity antibodies that bind to MAGE-A4, but not MAGE-02-0 BARS-VHC anslated peptide control (C) 45 MAGE-A4-MHC-binding from 23 cofres with secance deity was selected for high-throughou bodies expression and further characterization SUK Ow CYPAR VPS130 Ultra-specific, high-affinity MAGE-A4-pMHC binders Expanded peptido panel for hinding assessmen y RAM NMP TSPANS Sequence diversity Trouser VYA CHET indeva gras sprassin Figure 3. MAGE A4-MHC-binding antiboches a highly apsodio. (1) Antibody binding was further unga high-throughput peptide-pubed 12 way with MAGE-AAC and 13 other related pHC, including seven pHCG from the MAGE protein fomly one 13 MHC generated using the Selective Coes-Reactive Artgen Preton (RA) algorith. Practed indig ates of de to M-Csere calculated using Co. Rate MHC- levels in 12 colspused with different packs samasure of positive peptide binding 0 MHC-0 are shown, Peptides marked with were escladed due to week peotide-MHC-binding Qualitative binding met Ending kin Ⓒ MADEM MARE CHEL sro Col-binding assent P SARK Fe 2. MACE-A4-MHC-binding antibodies were identified (A) Ansbody binding was assessed using a multiplesed bead-besed binding validation assay with MAGE-A4-pHC and closely related MHCnding (>5F0D como MAGE-A4-MHC binding benchmark ort body and detected using flow cytometry Sensorgrams generated from Surface Plasmon Resonance (SPR kans of a selected target-binding asoodyshowtively strong binding to MNGE MHC compared to MAGE 48-CMHC No binding was observed to MAGE-83- or SARS-MO MMC 1 (8) High MAGE-MaMHC binding and bod en show high opty for MAGE A4 HC with low tone binding to the other posted Pepada panel for binding ment GRYPARENTY Oran PO PASTRECTH Binding affinity ⒸSPR FO Wil (C) body binding was further assessed in a Desde pused T2 with MAGE-A4-MC and closel edding 5 FOD was detected using tow Over 70% of antibodiested bound to both MAGE-A-HC and MAGE AD OMHC a closely related pepe expressed on tumor cells in both De y MHC- genopression lavals in 12 cella pulsed with forent optides (as a measure of povepose binding to MHC-ase show 101 (C) Senetic analysis of antibody binding to MAGE A4 CandMAGE ABMHC No anding was observed to M82 or SARS HO not shown Biophysical assem ICE 505 300 Developable antibodies with favorable biophysical properties En palam 200 AUTHORS Ce Toronto Bergant Tim Jacob Groce Lounge Vigo Antos Sarka, Harveer Chap We Shirley de Sal Gocean. Cindy Los Crichten Mal Ciel, Jessic Permende deure Kord A La Massene under Ar Conclusions & next steps REFERENCES F 100 min Wensbody diecosery and development ong nowo dod panel of diverse and develoosble antibodies that bind with high af affinity and high specificity to by recoma are specific for MAGE-44 o mation other pack that bind to MHC-with highatty have table developby 2 200 Body making Figure 4. MAGE-A4-MHC-binding antibodies have favoble developability profiles with high t med by capary gel electrophore using adum dadecyl CE-SDS), or aggregation med by absolute size exclusion chromatography 05 low relative surface drophobicity mesured by anatical hydrophobic interaction chromatography (C) high stability med brynars differentialing Buatry, low polyspecificity axed by baculovirus particle ayme-inkedimenty EVP-EUSAL and low oelf-association measured by offinit capture self-interactionnanosarticle spect (AC-SINS) with cores normalized to high and low controls LOG # 1891 POST APCSO CS Thats wilhe pared with our pr described fully human CD-binders to get Tell engagors for further dovolent. We w Sinfunctional devlopaty and specificity assays including tumor celling and cata biecificantibody develouably essensents deed 12 lainding with degradating thay apel of pain anon-sto Investigate potential off-laget closer high-resolution structural assessments of and body-Cin KEY HIGHLIGHTS Find ultra specific antibodies that are comparable or superior to clinical benchmarks#8Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 8 PARTNER-INITIATED PROGRAMS. One partner program against difficult target advances to the clinic. One molecule entered the clinic teva#9Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 9 PARTNER-INITIATED PROGRAMS. Helping partners reach their next value inflection point. AbCellera was a founding partner in Abdera, who just announced $142M in financing. First program program started in March 2021, and Abdera announced it plans to file an IND in 2024 for its first clinical candidate, a radiopharmaceutical for the treatment of cancer. First IND anticipated in 2024 Abdera Therapeutics#10Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 10 Capital allocation to maximize long-term value while minimizing risk. Forward integration to expand the capabilities of our engine, including manufacturing, regulatory, and clinical activities Develop technology to unlock new target classes and modalities, including, T-cell engagers, and GPCRs and ion channels Build the portfolio by advancing high- quality programs and partnerships#11o COPYRIGHT © ABCELLERA Q1 2023 FINANCIALS UPDATE#12FINANCIALS Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 12 Strong portfolio growth. Total # of Programs Under Contract 177 Total # of Discovery Partners 41 Cumulative # of Partnered Program Starts 110 100 90 80 70 60 50 40 30 20 10 O 101 ill 2015 2016 2017 2018 2019 2020 2021 2022 2023 Q1 WITHOUT downstream participation + WITH downstream participation 9 006 8 7 5 4 3 2 1 O Cumulative # of Molecules in the Clinic 9 2015 2016 2017 2018 2019 2020 2021 2022 2023 Q1 Note: Showing year-end figures, except for most-recent quarter. Historical results are not necessarily indicative of future results.#13FINANCIALS Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 13 Now 9 molecules in the clinic. MOLECULE bamlanivimab (LY-CoV555) bebtelovimab (LY-CoV1404) TAK-920/DNL919 NEW undisclosed undisclosed NBL-012 NBL-015/FL-301 NBL-020 IVX-01 STAGE Marketed, Emergency Use Authorization (EUA) Marketed, Emergency Use Authorization (EUA) Phase 1 Phase 1 Phase 1 Phase 1 Phase 1 IND/CTA authorized Clinical field study THERAPEUTIC AREA ● ● ● ● ● ● ● infectious disease: COVID- 19 infectious disease: COVID-19 neurology: Alzheimer's Disease neuroscience undisclosed dermatology gastrointestinal disease immunology oncology oncology animal health PARTNER Lilly DENALI teva undisclosed NovaRock BOTHERAPEUTICS Invetx PROGRAM TYPE AbCellera pre-partnered program PARTNERED AbCellera partner-initiated discovery Trianni license AbCellera partner-initiated discovery As of March 31, 2023#14FINANCIALS Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 14 $12M total revenue, driven by research fees from robust discovery activity. Revenue USD ROYALTIES MILESTONES LICENSING RESEARCH FEES $316.6M Q1 2022 $12.2M $10.6M Q1 2023 $1.3M#15FINANCIALS Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 15 Operating expenses reflect ongoing investments. Operating Expenses USD RESEARCH & DEVELOPMENT $26.4M Q1 2022 +$26.3M ↓ $52.6M Q1 2023 SALES & MARKETING $2.4M Q1 2022 +$1.4M $3.8M Q1 2023 GENERAL & ADMIN $14.3M Q1 2022 +$0.9M $15.1M Q1 2023#16FINANCIALS Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 16 Net loss of $40M; equivalent to ($0.14) per share (basic & diluted). Earnings USD NET EARNINGS $168.6M Q1 2022 -$40.1M Q1 2023 EARNINGS PER SHARE: BASIC $0.59 Q1 2022 -$0.14 Q1 2023 EARNINGS PER SHARE: DILUTED $0.54 Q1 2022 -$0.14 Q1 2023#17FINANCIALS Q1 2023 BUSINESS UPDATE COPYRIGHT © ABCELLERA 17 Over 800 million in total cash, equivalents, and marketable securities. Cash Flows USD $915M $500M Marketable Securities $387M Cash & Equivalents $28M* 31-Dec-22 ($44M) OPERATING $98M Marketable Securities (net) $51M Other ($150M) INVESTING $OM FINANCING * SOM FX $824M $603M Marketable Securities $193M Cash & Equivalents $27M* 31-Mar-23 Restricted cash (including restricted cash in other assets)#1818 COPYRIGHT © ABCELLERA Q1 2023 BUSINESS UPDATE YOU THANK

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