Inhibrx Biosciences, Inc. · NASDAQ:INBX
Inhibrx Biosciences — Investor Presentation (June 2024)
23 slides from Inhibrx Biosciences's investor presentation, June 2024
Slide 1: Investor Presentation
INHIBRX Investor Presentation Innovation Driven Outcomes Focused
Slide 2: Presentation disclaimer
Presentation disclaimer This presentation of Inhibrx Biosciences, Inc. (the “Company”) contains forward-looking 10-Q, and supplemented from time to time by our Current Reports on Form 8-K. The Company statements. In some cases, you can identify forward-looking statements by the words “will,” may not
Slide 3: Our company
Our company We aim to evolve into a commercial-stage Key financial highlights: biopharmaceutical company with (as of 5/30/2024) a differentiated and sustainable product To discover & develop portfolio by focusing on the following: effective biologic $255.4M Rapidly advance and optimize Cash and cash
Slide 4: Our company
Our company In-house expertise: Company snapshot: 160+ Discovery Biosciences employees with an experienced Protein engineering leadership team Cell biology $ Translational research 2024 INBRX-101 >300 Chemistry acquisition ozekibart (INBRX-109) by Sanofi Manufacturing and controls Patients treated 2
Slide 5: Inhibrx's innovative approach to therapeutic discovery
Inhibrx’s innovative approach to therapeutic discovery Our core belief: Our technology and protein engineering expertise enables us to efficiently identify optimal therapeutic formats bespoke to the target biology. Modular protein Rapid and iterative optimization process Therapeutics tailored to dis
Slide 6: Pipeline
Pipeline Phase 1 Phase 2 Phase 3 Milestones 1H 2025 + Precisely engineered valency to mediate optimal ozekibart Registration- balance of efficacy and safety. enabling Phase 2 (INBRX-109) Chondragon + Registration-enabling study in chondrosarcoma tetravalent underway. chondrosarcoma DR5 agonist + Exp
Slide 7: ozekibart (INBRX-109)
Goal: To develop a more precise DR5 agonist able to selectively induce apoptosis in tumor cells Empirically selected tetravalent DR5 agonist that restricts ozekibart unwanted secondary clustering (INBRX-109) tetravalent DR5 agonist DR5 agonists with limited on target effect or unwanted off tumor tox
Slide 8: ozekibart (INBRX-109): a next generation DR5 agonist
ozekibart (INBRX-109): a next generation DR5 agonist INBRX-109 with an optimized balance of efficacy and safety Death Receptor 5 (DR5 / TRAIL-R2) is highly expressed on ozekibart (INBRX-109) characteristics: tumorigenic, transformed or damaged cells but not normal cells, making DR5 a promising thera
Slide 9: ozekibart (INBRX-109): Phase 1 trial design
ozekibart (INBRX-109): Phase 1 trial design INBRX-109 Study of ozekibart (INBRX-109) in patients with locally advanced or metastatic solid tumors, including sarcomas (NCT03715933) Part 1 Part 3 ozekibart (INBRX-109) Dose expansion with chemotherapy single-agent dose escalation N=20 N=130 Completed M
Slide 10: Encouraging mPFS and clinical responses in chondrosarcoma patients
Encouraging mPFS and clinical responses observed in INBRX-109 Chondrosarcoma patients treated with ozekibart (INBRX-109) Impact of valency on DR5-mediated cell death Selected case reports PFS by Kaplan-Meier analysis Among evaluable chondrosarcoma patients (n=31), Partial response: the disease contr
Slide 11: Phase 2 registration enabling study in chondrosarcoma
ozekibart (INBRX-109) Phase 2 registration enabling study in INBRX-109 chondrosarcoma ozekibart (INBRX-109) N=134 Primary endpoint: 3 mg/kg every three weeks Progression free survival. Randomization stratified Ongoing Secondary endpoints: by line R of therapy, Overall survival, quality of life, over
Slide 12: ozekibart in combo with IRI/TMZ in Ewing sarcoma
ozekibart (INBRX-109) in combo with IRI/TMZ in metastatic, INBRX-109 unresectable Ewing sarcoma Best tumor response Efficacy PR Disease control rate was 76.9%, PR SD PR a Classical EWS Other RCS 76.9% or 10 out of 13 patients PR ozekibart (INBRX-109) (n=13)b Durable clinical benefitc as measured by
Slide 13: INBRX-106
Goal: strong To develop a potent OX40 agonist able to induce robust signal activation Hexavalent OX40 agonist with enhanced clustering/signaling INBRX-106 hexavalent OX40 agonist weak Bivalent OX40 agonists elicit weak downstream signals with limited clinical activity Previous generation Inhibrx sol
Slide 14: INBRX-106: generating robust OX40 signaling
INBRX-106: generating robust OX40 signaling to drive anti-tumor activity INBRX-106 INBRX-106 is designed to boost anti-tumor T-cell activity by INBRX-106 characteristics: potently activating the OX40 co-stimulatory pathway Simultaneously engage multiple Hexavalent OX40 to drive enhanced Six OX40 Sti
Slide 15: INBRX-106 study design
INBRX-106 study design INBRX-106 Phase 1/2 study of INBRX-106 ± pembrolizumab in adults with locally advanced or metastatic solid tumors—cohorts now enrolling Part 1 Part 2 Part 3 Part 4 INBRX-106 INBRX-106 Dose escalation INBRX-106 single-agent single-agent with dose expansion dose escalation dose
Slide 16: Seamless Phase 2/3 study of INBRX-106 with pembrolizumab in 1L HNSCC
Seamless Phase 2/3 study of the hexavalent OX40 agonist INBRX-106 INBRX-106 with pembrolizumab in 1L R/M HNSCC with PD-L1 CPS ≥20 Gating Survival Phase 2, Phase 3, Phase 2/3 Follow-up Open label Double blind Criteria: + cORR + DOR Co-primary endpoint: INBRX-106 + CBR INBRX-106 Key inclusion criteria
Slide 17: Investor Relations
Investor Relations: KELLY DECK, CPA CFO 11025 N. Torrey Pines Road Suite 140 La Jolla, CA 92037 858.795.4260 ir@inhibrx.com
Slide 18: Appendix
Appendix 18
Slide 19: ozekibart is a potent inducer of extrinsic cell death via DR5
ozekibart (INBRX-109) is a potent inducer INBRX-109 of extrinsic cell death via the DR5 pathway TRAIL ozekibart (INBRX-109) DR5 DR5 DR5 FADD FADD FADD Tumor cell Caspase activation Tumor cell Caspase activation Tumor cell Caspase activation Apoptosis moderate strong Apoptosis Apoptosis DR5 (TRAIL-R2
Slide 20: ozekibart is precision-engineered for optimal potency and safety
ozekibart (INBRX-109) is precision-engineered INBRX-109 for optimal potency and safety Valency drives both DR5-induced tumor cell death and hepatocyte destruction Impact of valency on DR5-mediated cell death Impact of valency on hepatotoxicity Impact of valency on cell death: Impact of valency on ce
Slide 21: INBRX-106: mechanism of action
INBRX-106: mechanism of action INBRX-106 Effective OX40 agonism potentiates the body’s immune response towards a tumor T cell ↑ T cell TTcells cells TT ↑OX40 OX40 NK NKcells cells NK NK TCR TCR antigen antigen INBRX-106 Tumor MHC MHC Monocytes Monocytes Dendritic cell Tumor cell Tumor cell The T-Cel
Slide 22: Higher OX40 valency drives superior T cell activation
Higher OX40 valency drives superior T cell activation INBRX-106 and reduces Treg suppression CD4 T Cell Co-Stimulation1 Reversal of Treg Suppression2 ~2-fold increase vs bi-valent and untreated CD8 T Cell Co-Stimulation1 Hexavalent INBRX-106 engagement drives superior co-stimulation of both CD4 and
Slide 23: Valency drives OX40 agonism in CPI-resistant tumor models
Valency drives OX40 agonism in CPI-resistant tumor models INBRX-106 Syngeneic B16F10 Mouse Tumor Model Vehicle Bivalent OX40 mAb Hexavalent INBRX-106-a* OX40 agonism upregulates PD-L1 expression on CD4 and CD8 T-cells supporting rationale of 0/10 CRs 0/10 CRs 3/10 CRs combination with anti-PD1 agent
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