INHIBRX Investor Presentation Innovation Driven Outcomes Focused
2 Presentation disclaimer This presentation of Inhibrx Biosciences, Inc. (the “Company”) contains forward-looking statements. In some cases, you can identify forward-looking statements by the words “will,” “expect,” “intend,” “plan,” “objective,” “believe,” “estimate,” “potential,” “continue” and “ongoing,” or the negative of these terms, or other comparable terminology intended to identify statements about the future. These statements are based on management’s current beliefs and expectations. These statements include but are not limited to statements regarding the Company’s business strategy, the Company’s plans to develop and commercialize its product candidates, the safety and efficacy of the Company’s product candidates, the Company’s plans and expected timing with respect to clinical trials and regulatory filings and approvals, manufacturing matters, strength of intellectual property protection, and the size and growth potential of the markets for the Company’s product candidates, and any implication that pre- clinical data or preliminary or topline results will be representative of the results of later trials. This presentation also contains certain projections and estimates regarding the Company’s future financial performance, namely potential future revenue for certain of the Company’s product candidates. This information also constitutes forward-looking information and is for illustrative purposes only and should not be relied upon as necessarily being indicative of any future results. The assumptions and estimates underlying this estimated financial information are inherently uncertain and subject to a wide variety of significant business, economic competitive and other risks and uncertainties that could cause actual results to differ materially from those contained in the prospective financial information. These potential financial information and other forward- looking statements involve substantial known and unknown risks, uncertainties and other factors that may cause the Company’s actual results, levels of activity, performance or achievements to be materially different from the information expressed or implied by these forward-looking statements. Additional information regarding the Company’s risks and uncertainties are described from time to time in the “Risk Factors” section of our Securities and Exchange Commission filings, including those described in our Annual Report on Form 10-K as well as our Quarterly Reports on Form 10-Q, and supplemented from time to time by our Current Reports on Form 8-K. The Company may not actually achieve the plans, intentions or expectations disclosed in its forward-looking statements, and you should not place undue reliance on the Company’s forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements the Company makes. The forward- looking statements in this presentation represent the Company’s views as of the date of this presentation. The Company anticipates that subsequent events and developments will cause its views to change. However, while the Company may elect to update these forward-looking statements at some point in the future, the Company has no current intention of doing so except to the extent required by applicable law. You should, therefore, not rely on these forward-looking statements as representing the Company’s views as of any date subsequent to the date of this presentation. The investigational product candidates discussed in this presentation have not been approved or licensed by the U.S. Food and Drug Administration or by any other regulatory authority, and they are not commercially available in any market. This presentation also contains estimates and other statistical data made by independent parties and by the Company relating to market size and growth and other data about its industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such estimates. In addition, projections, assumptions, and estimates of the Company’s future performance and the future performance of the markets in which it operates are necessarily subject to a high degree of uncertainty and risk. The Inhibrx logo is a registered trademark of Inhibrx Biosciences, Inc. All third-party trademarks used herein are registered trademarks of their respective owners. This presentation shall not constitute an offer to sell or the solicitation of an offer to buy securities.
3 Our company To discover & develop effective biologic treatments for people with life-threatening conditions We aim to evolve into a commercial-stage biopharmaceutical company with a differentiated and sustainable product portfolio by focusing on the following: Rapidly advance and optimize clinical development. Key financial highlights: (as of 5/30/2024) Create differentiated, next-generation therapeutics in focused disease areas. Maintain our culture of innovation, execution and efficiency. Maximize the potential of our therapeutic pipeline. $255.4M Cash and cash equivalents $14.5M Common stock outstanding $19.1M Fully diluted outstanding
4 Our company In-house expertise: 160+ employees with an experienced leadership team >300 ozekibart (INBRX-109) Patients treated to date Discovery Protein engineering Cell biology Translational research Chemistry Manufacturing and controls Clinical development and operations Company snapshot: founded Biosciences 2018 first IND 2020 IPO 2024 INBRX-101 acquisition by Sanofi $ 2010 >175 INBRX-106 Patients treated to date Commercial
5 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. Therapeutics tailored to disease biologyRapid and iterative optimization processModular protein engineering platforms Single domain antibodies Recombinant proteins Engineered cytokines Multi-specific molecules Molecule binds to multiple targets allowing cross linking – a novel way of delivering the drug closer to where its needed Multi-valent molecules Molecule delivers higher clustering correlating with greater activity and more robust signal Engineered Fc Domains Fc-Fusion Proteins Endow proteins with antibody-like PK properties Affinity Biophysical properties Biological function Pharmacokinetic profile Developability / Manufacturability Therapeutic Format
6 Pipeline ozekibart (INBRX-109) tetravalent DR5 agonist INBRX-106 hexavalent OX40 agonist + Precisely engineered valency to mediate optimal balance of efficacy and safety. + Registration-enabling study in chondrosarcoma underway. + Expansion of Ewing cohort following preliminary efficacy data as shown at CTOS. Phase 1 Phase 2 Phase 3 + Robust OX40 agonist superior to bivalent antibodies. + Promising clinical activity in ongoing phase 1/2. + Cohort in NSCLC- SA and in combo with IO and chemotherapy. Milestones 1H 2025 Registration- enabling Phase 2 Chondragon chondrosarcoma data + 1H 2025 Phase 1 randomized, CPI r/r NSCLC data + 2H 2025 Phase 2 HNSSC initial data
ozekibart (INBRX-109) tetravalent DR5 agonist Previous generation Goal: To develop a more precise DR5 agonist able to selectively induce apoptosis in tumor cells Empirically selected tetravalent DR5 agonist that restricts unwanted secondary clustering DR5 agonists with limited on target effect or unwanted off tumor toxicity Inhibrx solution
8 INBRX-109 ozekibart (INBRX-109): a next generation DR5 agonist with an optimized balance of efficacy and safety Death Receptor 5 (DR5 / TRAIL-R2) is highly expressed on tumorigenic, transformed or damaged cells but not normal cells, making DR5 a promising therapeutic target in oncology1-4 ozekibart (INBRX-109) characteristics: Prevents cross-linking and higher order clustering IgG Fc Fc engineered to minimize effector function Four DR5 sdAbs Empirically selected and engineered to avoid ADAs Tumor Cell Apoptosis Caspase C Programmed Cell Death C Tetravalent Empirically designed to simultaneously engage four DR5 molecules Immunogenic Epitopes removed Prevents unwanted higher order clustering via anti-drug antibodies Prevents higher order clustering and allows for antibody-like PK Effector Disabled Fc sdAb backbone limits molecule size (106 kDa) which may allow for better tumor penetration Smaller Size 1. Mol Cancer Ther. 2012;11(11):2541-2546. 2. Cancer Cell. 2014;26(2):177-189. 3. Haematologica. 2005;90(5):612-624. 4. Cell Res. 2005;15(6):430-438
9 INBRX-109 ozekibart (INBRX-109): Phase 1 trial design N=20 N=116 Dose expansion with chemotherapy N=130 Part 3 Completed Completed Part 2 ozekibart (INBRX-109) single-agent dose expansion ozekibart (INBRX-109) single-agent dose escalation Part 1 Study of ozekibart (INBRX-109) in patients with locally advanced or metastatic solid tumors, including sarcomas (NCT03715933) Mesothelioma Pancreatic adenocarcinoma Colorectal adenocarcinoma Ongoing Ewing sarcoma RP2D: INBRX-109 3mg/kg + IRI 50 mg/m2/day + TMZ 100 mg/m2/day N=50 RP2D: INBRX-109 3mg/kg + TMZ 100 mg/m2/day Safety lead-in SDH-def solid N=20 Primary endpoint all: safety (AEs and DLTs). Secondary endpoints all: pharmacokinetics and immunogenicity (ADAs). Exploratory endpoints all: clinical response, predictive diagnostic biomarkers. Primary endpoints Ewing: Clinical response, including ORR and DOR per RECIST 1.1. Secondary endpoints Ewing: PFS.
10 INBRX-109 Encouraging mPFS and clinical responses observed in Chondrosarcoma patients treated with ozekibart (INBRX-109) Impact of valency on DR5-mediated cell death IDHmt, isocitrate dehydrogenase 1/2 mutant; PFS, progression-free survival. a Includes 1 patient from dose-escalation cohort A4 (INBRX-109 10 mg/kg) and 22 patients from dose-expansion cohort B4 (INBRX-109 3 mg/kg); b Two patients were excluded due to taking prohibited medication (n=1) or having dedifferentiated chondrosarcoma (n=1). Among evaluable chondrosarcoma patients (n=31), the disease control rate (DCR) was 87.1% (27/31) + 2 patients achieved PR (objective response rate, 6.5%), and 25 patients SD (80.6%) + Of those who experienced SD, 13 (52.0%) had decreases from baseline in tumor size + 29-year-old white male, histologic Grade 3 + 61% decrease in target lesions (RECISTv1.1) + Patient was on study for 45 weeks + 55-year-old white male, histologic Grade 3 + 24% decrease in target lesions (RECISTv1.1) + Patient was on study for 77 weeks Selected case reports Partial response: March 4, 2020 (baseline) April 29, 2020 September 3, 2020 (-61%) September 4, 2020 (-20%) Stable disease: Overall median PFS: 7.6 months (range, 0.03-17.8 mo) vs. <4 months historically1-3 1. van Maldegem A, et al. Oncologist 2019;24(1):110–6. 2. Livingston JA, et al. Oncotarget 2016;7(39):64421–30. 3. Duffaud F, et al. Eur J Cancer 2021;150:108–18. 4. NCCN. Bone cancer version 2.2022. 5. Tap WD, et al. J Clin Oncol. 2020;38(15):1693-1701. 6. Chow W, et al. Cancer. 2020;126(1):105-111. Although no approved agents, current guideline recommended treatment options4 have demonstrated modest activity as measured by RECIST criteria + ivosidenib resulted in no CR or PR, an SD rate of 52% in patients with advanced chondrosarcoma (n=21)5 + pazopanib in patients with unresectable or metastatic conventional chondrosarcoma (N=47) reported a DCR of 43% at week 166 PFS by Kaplan-Meier analysis
11 INBRX-109 ozekibart (INBRX-109) Phase 2 registration enabling study in chondrosarcoma + FDA fast track designation and orphan-drug designation + EMA orphan-drug designation Patients: R 2:1 Conventional chondrosarcoma, Grades 2 and 3, unresectable or metastatic. ozekibart (INBRX-109) Placebo 3 mg/kg every three weeks 3 mg/kg every three weeks N=134 N=67 Ongoing Ongoing Randomization stratified by line of therapy, Grade and IDH1/2 mutation status Completion projected 2H 2024 Primary endpoint: Progression free survival. Secondary endpoints: Overall survival, quality of life, overall response rate, duration of response, disease control rate, safety, etc. DSMB reviewed interim analyses in April 2024 and made the recommendation for trial continuation
12 INBRX-109 ozekibart (INBRX-109) in combo with IRI/TMZ in metastatic, unresectable Ewing sarcoma Efficacy Disease control rate was 76.9%, or 10 out of 13 patients as measured by RECISTv1.1. + Most common adverse events (diarrhea, nausea, and fatigue) were consistent with the known safety profile of IRI/TMZ + One patient had increased alanine aminotransferase (grade 1); no other liver-related AEs were reported Safety 20 0 -20 -40 -60 -80 Ch an ge fr om b as e lin e, % Progressive disease Partial response Best change from baseline in tumor size Classical EWS Other RCS ozekibart (INBRX-109) (n=13)b Best overall response, n (%) PR 7 (53.8) SD 3 (23.1) ORR, n (%) 7 (53.8) DCR, n (%) 10 (76.9) Best tumor response Months 0 6 12 a PR PR SD PR PR PR PR SD PD PR PD SD PD Classical EWS Other RCS Durable clinical benefitc Response start Response end PD Patient censored Ongoing progression- free patient Data cutoff: September 8, 2023. CR, complete response; DCR, disease control rate; EWS, Ewing sarcoma; ORR, objective response rate; PD, progressive disease; PR, partial response; RCS, round cell sarcoma; SD, stable disease; AE, adverse event. a Patient discontinued treatment to undergo tumor resection surgery. b One patient had not reached the first set of restaging scans and was considered nonevaluable. c Durable clinical benefit was defined as having SD, PR, or CR for >6 months. Best response prior to progression is displayed; however, if a patient’s first scan result was progressive disease, then that result is displayed. EWS, Ewing sarcoma; RCS, round cell sarcoma. 7 patients who achieved partial responses (53.8%), 5 of which were observed in classical EWS patients (71.4%) and 2 of which were observed in RCS patients (33.3%) 76.9% 53.8%
INBRX-106 hexavalent OX40 agonist Hexavalent OX40 agonist with enhanced clustering/signaling Bivalent OX40 agonists elicit weak downstream signals with limited clinical activity Previous generation Goal: To develop a potent OX40 agonist able to induce robust signal activation weak strong Inhibrx solution
14 INBRX-106 INBRX-106: generating robust OX40 signaling to drive anti-tumor activity INBRX-106 is designed to boost anti-tumor T-cell activity by potently activating the OX40 co-stimulatory pathway Six OX40 sdAbs IgG Fc Hexavalent Simultaneously engage multiple OX40 to drive enhanced clustering/signaling Effector enabled Fc facilitates higher order clustering and greater downstream OX40 pathway signaling Non-Competitive Binding Complements natural ligand (OX40L) activity Facilitates higher order clusteringEffector Enabled Designed to agonize OX40 while allowing endogenous OX40L binding sdAb backbone limits molecule size (129 kDa) which may allow for better tumor penetration Smaller Size T cell Stimulation T cells NK cells Dendritic cellMonocytes T NK INBRX-106 characteristics:
15 INBRX-106 INBRX-106 study design ClinicalTrials.gov identifier, NCT04198766. Protocol version 7.0; March 5, 2024. a Chemo will be administered during the first 4 cycles. Pemetrexed can be continued after 4 cycles until progression or up to 35 cycles. Chemo, chemotherapy; CPI, checkpoint inhibitor; CPS, combined positive score; HNSCC, head and neck squamous cell carcinoma; M/R, metastatic/recurrent; NPC, nasopharyngeal carcinoma; NSCLC, non-small cell lung cancer; PD-L1, programmed cell death 1 ligand 1; pembro, pembrolizumab; q3w, every 3 weeks; R, randomization; R/R, relapsed/refractory; TMB, tumor mutational burden; TPS, tumor proportion score. Dose escalation with pembrolizumab INBRX-106 single-agent dose expansion INBRX-106 dose expansion with pembro ± chemo N=20 N=up to 70 N=up to 200 Part 1 Part 2 Part 4 Completed Completed Ongoing Ongoing NSCLC, PD-L1+ (TPS ≥50%) or TMB ≥10 mutations/Mb N=3-36 N=60 N=40 N=60 Key inclusion criteria: M/R NSCLC. <3 prior lines of therapy. PD-L1 TPS ≥50% or TMB ≥10 mutations/Mb. Alternating treatment INBRX-106 alternating Q3W with pembro Nonsquamous NSCLC INBRX-106 + pembro + pemetrexed + carboplatina Non-NPC and other Priming INBRX-106 loading dose → INBRX-106 + pembro Nonsquamous NSCLC INBRX-106 + pembro + pemetrexed + cisplatina NPC Concurrent INBRX-106 + pembro Squamous NSCLC INBRX-106 + pembro + (nab-)paclitaxel + carboplatina N=21 Part 3 Key inclusion criteria M/R HNSCC (non-NPC) or NPC. ≤1 prior line of chemotherapy in metastatic setting. PD-L1 CPS ≥1. Key inclusion criteria: M/R NSCLC Any prior line of therapy PD-L1 TPS ≥0% R 1:1:1 INBRX-106 single-agent dose escalation CPI R/R CPI naive CPI R/R or naive Phase 1/2 study of INBRX-106 ± pembrolizumab in adults with locally advanced or metastatic solid tumors—cohorts now enrolling
16 INBRX-106 Seamless Phase 2/3 study of the hexavalent OX40 agonist INBRX-106 with pembrolizumab in 1L R/M HNSCC with PD-L1 CPS ≥20 ClinicalTrials.gov identifier, NCT06295731. Protocol version 1.0; January 31, 2024. INBRX-106 to be administered every 3 weeks. Pembro 200 mg to be administered every 3 weeks. 1L, first line; CBR, clinical benefit rate; cORR, confirmed objective response rate; CPS, combined positive score; DOR, duration of response; ECOG PS, Eastern Cooperative Oncology Group performance status; HNSCC, head and neck squamous cell carcinoma; HPV, human papillomavirus; OS, overall survival; PD-L1, programmed cell death 1 ligand 1; pembro, pembrolizumab; PFS, progression-free survival; PFS6mo, progression-free survival rate at 6 months; PRO, patient-reported outcome; R, randomization; R/M, recurrent/metastatic; TTCx, time to chemotherapy; Tx, treatment. Phase 2, Open label Phase 3, Double blind Survival Follow-up Ongoing Ongoing INBRX-106 + Pembro INBRX-106 + Pembro Pembro Pembro Randomization will be stratified by: + Disease status (locoregional advanced vs metastatic). + HPV status (positive vs negative). + ECOG PS (0 vs 1). Co-primary endpoint: PFS and OS. Secondary endpoints: cORR, DOR, CBR, TTCx, safety, PROs. Gating Phase 2/3 Criteria: + cORR + DOR + CBR + PFS6m + safetyR 1:1 R 1:1 Key inclusion criteria: R/M HNSCC PD-L1 CPS ≥20 HPV status confirmed No prior systemic Tx for R/M HNSCC
Investor Relations: KELLY DECK, CPA CFO 11025 N. Torrey Pines Road Suite 140 La Jolla, CA 92037 858.795.4260 ir@inhibrx.com
18 Appendix
19 INBRX-109 ozekibart (INBRX-109) is a potent inducer of extrinsic cell death via the DR5 pathway Ozekibart (INBRX-109), a tetravalent DR5 agonist, is designed to simultaneously engage four DR5 molecules to drive enhanced clustering/signaling in tumor cells while minimizing off-target effects Apoptosis Tumor cell DR5 TRAIL FADD Caspase activation moderate strong Apoptosis Tumor cell ozekibart (INBRX-109) DR5 FADD Caspase activation DR5 (TRAIL-R2) is a pro-apoptotic receptor for TRAIL that is widely expressed on the surface of damaged, transformed or tumor cells, but rarely and at low levels on normal cells.1-4 TRAIL selectively induces programmed cell death via activation of the FADD and downstream caspase pathway, therefore playing an important role in tumor and viral immune surveillance5 Apoptosis Tumor cell DR5 FADD Caspase activation While the DR5 trimer is the minimal functional unit for TRAIL activity, clustering of multiple receptors at the cell-cell interface results can generate more potent apoptotic activity6-8 1. Mol Cancer Ther. 2012;11(11):2541-2546. 2. Cancer Cell. 2014;26(2):177-189. 3. Haematologica. 2005;90(5):612-624. 4. Cell Res. 2005;15(6):430-438. 5. Antibodies (Basel). 2017;6(4) 6. J Biol Chem. 2012;287(25):21265-21278. 7. Cell. 2019;176(6):1477-1489.e1414. 8. Proc Natl Acad Sci U S A. 2015;112(18):5679-5684.
20 INBRX-109 ozekibart (INBRX-109) is precision-engineered for optimal potency and safety Ab (nM) 100 InSphero 3D inSightTM human liver microtissue model: 75 50 25 1 10 100 Impact of valency on cell death: Impact of valency on DR5-mediated cell death ozekibart (INBRX-109) tetravalent Hexavalent DR5 hexavalent Impact of valency on hepatotoxicity 10-110-210-310-410-510-6 0 He pa to cy te v ia bi lit y (% ) Impact of valency on cell death: 125 Valency EC 50 (p M ) 4 62 3 1000 100 10 1 0.1 5.78x 6.35x 94.2x 10000 ozekibart (INBRX-109) tetravalent TRAIL trivalent Hexavalent DR5 hexavalent anti DR5 mAb bivalent 0.1 1 10 100 75 50 25 0 100 10000.010.0010.0001 % C el l d ea th Test article (nM) Valency drives both DR5-induced tumor cell death and hepatocyte destruction
21 INBRX-106 INBRX-106: mechanism of action The T-Cell Receptor (TCR) recognizes a tumor-associated antigen presented via MHC. In response, OX40 is upregulated on tumor reactive TILs facilitating an immune response directed towards the tumor. Effective OX40 agonism potentiates the body’s immune response towards a tumor Due to its six OX40 sdAb domains, binding of hexavalent INBRX-106 facilitates higher order clustering versus bivalent and tri-valent endogenous OX40L amplifying the downstream costimulatory signal. Costimulatory signaling via OX40 and the TCR-MHC receptors induce survival and proliferation of activated antigen-specific CD4 T cells, increases memory T cell generation, CD8+ effector T cells, and suppress the inhibitory capacity of regulatory T cells. T cells NK cells Monocytes Dendritic cell Tumor T NK T cells NK cells Monocytes T cell TCR MHC antigen Tumor cell ↑OX40 TCR MHC antigen Tumor cell OX40 INBRX-106 ↑ T cell
22 INBRX-106 Higher OX40 valency drives superior T cell activation and reduces Treg suppression Hexavalent INBRX-106 engagement drives superior co-stimulation of both CD4 and CD8 T-cells versus bi-valent OX40 mAbs INBRX-106, but a not bivalent OX40 mAb, reduces regulatory T-cell (Treg) mediated suppression of effector T-cells (Teff) ~2-fold increase vs bi-valent and untreated Reversal of Treg Suppression2 CD8 T Cell Co-Stimulation1 CD4 T Cell Co-Stimulation1 1. T-cell activation monitored by assessing CD71 expression following suboptimal anti-CD3-mediated stimulation 2. Reversal of Treg suppression assessed by CD25 upregulation following anti-CD3 stimulation
23 INBRX-106 Valency drives OX40 agonism in CPI-resistant tumor models Syngeneic B16F10 Mouse Tumor Model OX40 agonism upregulates PD-L1 expression on CD4 and CD8 T-cells supporting rationale of combination with anti-PD1 agents Hexavalent INBRX-106-a* demonstrated single-agent, single-dose activity in checkpoint- inhibitor responsive and resistant syngeneic tumor models INBRX-106-a* induced more robust anti-tumor activity as single agent and in combination with anti-PD1 0/10 CRs 1/10 CRs0/10 CRs 0/10 CRs 6/10 CRs 3/10 CRs Vehicle Bivalent OX40 mAb Hexavalent INBRX-106-a* Anti-PD1 Alone Anti-PD1 + Bivalent OX40 mAb Anti-PD1 + Hexavalent INBRX-106-a* *INBRX-106 mouse surrogate