Inhibrx Biosciences, Inc. · NASDAQ:INBX
Inhibrx Biosciences — Investor Presentation (October 2025)
35 slides from Inhibrx Biosciences's investor presentation, October 2025
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 mission: discover and develop effective biologic treatments
Our mission: To discover & develop effective biologic treatments for people with life-threatening conditions Key financial highlights: (as of 6/30/2025) >300 ozekibart (INBRX-109) $186.6M ~130 Patients treated to date Cash and cash employees with Biosciences equivalents an experienced >175 leadershi
Slide 4: 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 5: 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 6: ozekibart Clinical Data
ozekibart Clinical Data (INBRX-109) tetravalent DR5 agonist
Slide 7: Phase 1 data in unresectable or metastatic conventional chondrosarcoma
Phase 1 data in unresectable or metastatic conventional chondrosarcoma INBRX-109 Response SD × SD ► SD ► SD × SD × SD ○ SD ► SD × SD ► SD × SD × ** SD × SD × SD × SD × PR ▲ × SD × SD × SD × SD × SD × * SD × * SD ○ PR ▲ × SD ○ SD ○ SD × SD × SD × SD × Nonconventional chondrosarcoma ORR, n (%) 2 (3.7)
Slide 8: Topline results from registrational trial in conventional chondrosarcoma
Topline results from registrational trial in unresectable or INBRX-109 metastatic conventional chondrosarcoma Patients: Conventional chondrosarcoma, Grades 2 and 3, unresectable or metastatic. Primary endpoint met: Randomization stratified by line of therapy, Grade and IDH1/2 mutation status • HR= 0
Slide 9: Ongoing phase 1/2 trial in Ewing sarcoma and colorectal adenocarcinoma
Ongoing phase 1/2 trial in Ewing sarcoma and colorectal adenocarcinoma INBRX-109 CRC 3-4L with FOLFIRI Key inclusion N=50 criteria • LA/M, unresectable, R/R colorectal adenocarcinoma Ozekibart 3 mg/kg + FOLFIRI Primary endpoints: • Aged 18 to <85 years (FU, 2400 mg/m2; Clinical response, including •
Slide 10: Early results in colorectal adenocarcinoma with FOLFIRI
Early results in colorectal adenocarcinoma in combination with FOLFIRI INBRX-109 Response and time on treatment Efficacy Response (No. of prior LOTs) CR (3) + Of the 13 patients who received ozekibart, 4 had responses SD (1) (30.8%; partial response, n=3; complete response, n=1) PR (4) SD (3) – One
Slide 11: Expansion cohort: colorectal adenocarcinoma with FOLFIRI
Expansion cohort: colorectal adenocarcinoma in combination with FOLFIRI INBRX-109 40 20 PD Recruitment completed 44 patients dosed with 26 patients currently evaluable for response Change from baseline, % 0 -20 N=44 + 70% are 4th line & 30% are 3rd line PR + >80% have received prior IRI-containing -
Slide 12: Early results in phase 1 metastatic, unresectable Ewing sarcoma
Early results in phase 1 metastatic, unresectable Ewing sarcoma INBRX-109 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 RECISTv1.1. PR Best ov
Slide 13: Expansion cohort: Ewing sarcoma with IRI/TMZ
Expansion cohort: Ewing sarcoma in combination with IRI/TMZ INBRX-109 80 Recruitment ongoing 60 33 patients dosed with 25 patients currently evaluable for response: Change from baseline, % 40 PD N=33 20 0 Disease control rate was 92%, -20 PR 92% or 23 out of 25 patients, as measured by RECISTv1.1. -
Slide 14: Ozekibart anti-tumor activity in GBM models
Ozekibart exhibits anti-tumor activity in GBM models INBRX-109 as monotherapy and in combination with TMZ Human GBM cell line models In vitro cytotoxicity In vitro cytotoxicity Intracranial U-87 MG Intracranial U-87 MG + Combination treatment with INBRX-109 U-87 MG GBM cell lines Survival analysis S
Slide 15: Ozekibart Preclinical data and MOA
Preclinical data and MOA Ozekibart (INBRX-109) tetravalent DR5 agonist
Slide 16: ozekibart is a potent inducer of extrinsic cell death via DR5 pathway
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 17: Next generation DR5 agonist with optimized balance of efficacy and safety
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 18: 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 19: ozekibart is a best-in-class DR5 agonist with no competition
ozekibart (INBRX-109) is a best-in-class DR5 agonist with no competition INBRX-109 CANDIDATE VALENCY SIZE (KDA) STATUS INBRX-109 Tetravalent 105 Ongoing TAS-266* Tetravalent 60 Terminated Eftozanermin alpha (TRAIL-Fc Hexavalent 167 Terminated fusion) GEN1029 Dodecavalent 150 ka (2x mAbs) Terminated
Slide 20: INBRX-106
Goal: To develop a potent OX40 agonist able to induce robust signal activation strong strong 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 Inhi
Slide 21: INBRX-106 Clinical Data
INBRX-106 Clinical Data hexavalent OX40 agonist
Slide 22: INBRX-106 is a biologically active drug in patients
INBRX-106 is a biologically active drug in patients INBRX-106 Max fold change from baseline in percentage of Ki-67+ memory cells CD4+ 15 15 T-cells 10 10 Observed PD consistent with T-cell co- stimulation by INBRX-106 5 5 INBRX-106 induced dose-dependent 0 0 proliferation of CD4+ and CD8 + memory T-
Slide 23: Phase 1 data: PD-L1+ CPI-R/R or CPI-naive HNSCC
Phase 1 data: PD-L1+ CPI-R/R or CPI-naive HNSCC INBRX-106 INBRX-106 with pembrolizumab 60 Cohort CPI-naïve (F4) 40 CPI-R/R (F1) NPC* patient (D2) PD 20 Best change from baseline, % 0 -20 PR -40 -60 -80 -100 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 PD-L1 CPS 0 100 0 30 1 10 75 20 100 100 10 5 24 90 25 + T
Slide 24: Phase 1 data: PD-L1+ CPI-R/R NSCLC
Phase 1 data: PD-L1+ CPI-R/R NSCLC INBRX-106 INBRX-106 with pembrolizumab 60 40 Cohort F2 20 PD Change from baseline, % 0 -20 PR -40 -60 -80 -100 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 19 19 20 21 22 23 24 25 26 PD-L1 TPS 60 20 95 10 80 80 90 2 11 20 3 75 10 10 35 1 50 1 1 10 41 100 50 60 100 90
Slide 25: Seamless Phase 2/3 study in 1L R/M HNSCC
Seamless Phase 2/3 study in 1L R/M HNSCC with PD-L1 CPS ≥20 INBRX-106 INBRX-106 with pembrolizumab Phase 2 data readout expected Q4 2025 Proof of concept study: If successful in HNSCC, has the potential to work broadly against all approved checkpoint indications Phase 2, Phase 3, Survival Randomizat
Slide 26: Ongoing Phase 1/2 trial in NSCLC and HNSCC
Ongoing Phase 1/2 trial in metastatic/recurrent NSCLC and HNSCC INBRX-106 Readouts expected Q4 2025 NSCLC: CPI relapsed/refractory Primary endpoints: + Objective response rate (ORR) per Response Evaluation Key inclusion criteria N=60 Criteria in Solid Tumors (RECIST) version 1.1 and iRECIST, disease
Slide 27: INBRX-106 Preclinical Data and MOA
strong INBRX-106 Preclinical Data and MOA hexavalent OX40 agonist
Slide 28: 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 29: OX40 T-cell costimulation validated by antagonists in autoimmune disease
OX40 T-cell costimulation in human disease is validated by OX40 INBRX-106 antagonists in autoimmune disease An anti-OX40 antibody to treat moderate-to-severe atopic dermatitis: a multicenter, double-blind, placebo-controlled phase 2b study 29 Lancet 2023; 401: 204–14
Slide 30: INBRX-106 designed to maximize OX40 signaling activation strength
INBRX-106: uniquely designed to maximize OX40 signaling activation INBRX-106 strength, leading to enhanced t-cell-driven anti-tumor activity INBRX-106 is designed to boost anti-tumor T-cell activity by INBRX-106 features: maximizing the strength of the OX40 co-stimulatory pathway Simultaneously enga
Slide 31: Receptor hyperclustering induces stronger OX40 signaling
Receptor hyperclustering induces stronger OX40 signaling and more INBRX-106 effective t-cell-driven anti-tumor activity Pathway T-cell proliferation activation OX40 OX40L T-cell survival T-cell differentiation Tumor cell Signaling Enhanced trafficking of death through T cells to the tumor OX40 Robus
Slide 32: INBRX-106 drives superior CD4+ and CD8+ T-cell activation
INBRX-106 drives superior CD4+ and CD8 + 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
Slide 33: Hexavalent OX40 and PD-1 combination enhanced anti-tumor activity
Hexavalent OX40 and PD-1 antibody combination results in enhanced anti- INBRX-106 tumor activity in CPI-resistant tumor models 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
Slide 34: INBRX-106 first and potentially best-in-class multi-valent OX40 agonist
INBRX-106 is a first and potentially best-in-class multi-valent OX40 agonist INBRX-106 CANDIDATES VALENCY STATUS INBRX-106 Hexa- Phase 2/3 GEN1055/BNT315 Dodeca- Phase 1 MOXR-0916 Bi- Terminated GSK-3174998 Bi- Terminated BMS-986178 Bi- Terminated INCAGN-1949 Bi- Terminated ABBV-368 Bi- Terminated I
Slide 35: 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
Inhibrx Biosciences — Investor Presentation (October 2025) on 6ix