inhibrxpresentationaugus

INBX Investor Presentation Outcomes Focused August 2023 Innovation Driven

2 Presentation disclaimer This presentation 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 Inhibrx, Inc.’s (the “Company”) 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. Inhibrx, the Inhibrx logo and ContraMAB are registered trademarks of Inhibrx, 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 IPO in 2020 First IND in 2018 Founded in 2010 Company overview Partnerships with Industry Leaders: 165+ employees with an experienced leadership team and a deep expertise in protein engineering $192.5M Cash and cash equivalentsKey Financial Highlights: (as of 6/30/2023) 43.7M Common stock outstanding 50.8M Fully diluted outstanding > 30% Internal ownership

4 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 biology Rapid and iterative optimization process Modular 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

5 Pipeline Oncology: INBRX-109 tetravalent DR5 agonist INBRX-106 hexavalent OX40 agonist INBRX-105 tetravalent PD-L1 targeted 4-1BB agonist Preclinical Phase 1 Phase 2 Phase 3 Precisely engineered valency to mediate optimal balance of efficacy and safety Registration-enabling study in chondrosarcoma underway Robust OX40 agonist superior to bivalent antibodies Promising clinical activity in ongoing phase 1/2 Randomized, Phase 2 study in CPI r/r NSCLC- SA and in combo with IO; update in Q4 ’23 with data expected 2H ‘24 Elicits 4-1BB agonism and enhanced T-cell response localized to PD-L1 rich tumor micro-environment Promising clinical activity in ongoing phase 1/2 Phase 2 study CPI r/r HNSCC in process; data expected 1H ‘24 Registration Study Registration StudyINBRX-101 recombinant Alpha-1 antitrypsin Fc-fusion protein (AAT-Fc) Anti- Inflammatory / Rare disease: Optimized to achieve and maintain normal functional Alpha-1 antitrypsin levels with less frequent dosing Registration-enabling studies in AATD underway De-risked opportunity in GvHD with studies beginning in Q4 ‘23/Q1 ‘24 Other Programs on the Horizon FcRN Antagonist Radiopharmaceuticals T-cell Engagers - ContraMAB® Platform γδ T-cell Targeted Cisleukin™ Molecule

6 Near term expected clinical milestones 2H 2023 1H 2024 (PD-L1x41BB) Single agent data in r/r HNSCC INBRX-109 (DR5) Initial mesothelioma, Ewing sarcoma, colorectal cancer and GIST combination study data INBRX-101 (GvHD) Trial initiations for aGvHD and cGvHD INBRX-109 (DR5) Registration-enabling Phase 2 Chondrosarcoma data INBRX-105 INBRX-106 (OX40) Randomized, CPI r/r NSCLC data 2H 2024 INBRX-101 (AATD) Initial readout from ElevAATe study (OX40) Keytruda combination update INBRX-106

INBRX-101 AATD recombinant Alpha-1 antitrypsin Fc-fusion protein (AAT-Fc) Recombinant AAT protein Plasma Donor derived AAT protein Goal: To develop a donor-independent source of AAT protein able to keep patients in the range of normal for extended periods of time Current SOC Inhibrx solution AAT

8 INBRX-101 INBRX-101 for the treatment of alpha-1 antitrypsin (AAT) deficiency (AATD) Liver Hepatocytes synthesize and secrete AAT into the blood stream Lung AAT protects from lung tissue damage AAT protein inactivates neutrophil elastase thus preventing elastin degradation. AATD: Without AAT protein, elastase activity is unchecked and causes damage to the lung tissue and restricts airflow. Disease background AATD is an inherited rare disease of the lungs and liver (~15% of cases) characterized by low levels of AAT protein, a neutrophil elastase inhibitor, causing progressive deterioration of the tissue. Current standard of care Weekly augmentation of plasma donor derived AAT (pdAAT) brings patients to roughly half the normal level Lung cell AAT protein Elastin AAT protein Pi*Z and PI*S alleles cause the majority of severe AATD cases ZZ Healthy: SZ Elastase Lung cell

9 INBRX-101 INBRX-101 for the treatment of AATD AAT two recombinant human AAT proteins IgG4 Fc Sustainable supply Purified product Less frequent dosingProvides patients with normal level of protein for up to 3-4 weeks Not dependent on plasma donation Independent of risks associated with blood derived products Better quality of life Prevents loss of activity in the lungs Oxidation- prone residues eliminated INBRX-101 is a precisly engineered recombinant human AAT-Fc fusion protein INBRX-101 characteristics: Extended half-life Normalization of AAT levels Dosed to keep patients in the healthy normal range

10 INBRX-101 INBRX-101: phase 1 study design INBRX-101 phase 1 study: open-label, multicenter, dose-escalating study Adult patients with AATD, regardless of prior treatment with augmentation therapy AAT serum concentration <11 µMa Nonsmoker N=6 N=6 N=6 40 mg/kg 80 mg/kg* 120 mg/kg* 40 mg/kg 80 mg/kg 120 mg/kg N=6 N=6 N=6 Complete Complete Each patient receives 3 doses, Q3WOne dose N=18N=24 N=6 10 mg/kg Eligibility Part 1 Part 2 Parts 1 and 2: Single ascending dose (SAD) Multiple ascending dose escalation (MAD) Part 2 80 and 120-mg/kg cohorts: Postbronchodilator FEV1 of ≥40% of predicted normal value * bronchoalveolar lavage Primary endpoint: Safety & tolerability of INBRX-101, determined by the frequency & severity of adverse events Secondary endpoints: Pharmacokinetics, pharmacodynamics, and immunogenicity of INBRX-101

11 INBRX-101 Topline results from phase 1, part 2 Parts 2: Favorable safety and tolerability profile with only mild and a few moderate AEs that were transient and fully reversible with minimal or no symptomatic care Dose related increases in maximal and total exposure occurred across entirety of SAD and MAD ranges of 10-120 mg/kg. Overall, antidrug antibodies (ADAs) had no significant impact on INBRX-101 PK INBRX-101 topline results – 3rd dose of 40, 80 or 120 mg/kg (Q3W): MAD cohorts demonstrate observed Cavg of functional AAT of 37.6 µM and 45.4 µM over the 21-day dosing interval following the third 80 mg/kg and 120 mg/kg doses, respectively. In contrast, fAAT levels from PiMM genotype healthy volunteers (n=65) ranged from 21 to 54 micromolar (µM), with a mean of 36 µM. fAAT levels at Day 70 (28 days following the 3rd dose), on average, were within the normal range for the 120 mg/kg dose level. Fu nc tio na l A AT le ve ls (μ M ) Time (days) Indicates timing after third dose * Baseline values shown at Day 0 Baseline: 120 mg/kg 80 mg/kg 40 mg/kg 14 2821 40 100 60 80 20 0 0 7 Healthy (PiMM) Normal Range

12 INBRX-101 INDRX-101 is present in the lung in every patient sampled following IV dosing suggesting penetration to target organ 100 Day 56 IN BR X- 10 1 (μ g/ m L) 0 50 200 150 120 mg/kg 80 mg/kg naive rollover naive rollover Bronchoalveolar lavage fluid (BALF) sample collection and analysis BALF samples were collected from 3 lobes of the lung for each patient in the 80 (N = 5) and 120 (N = 6) mg/kg MAD cohorts prior to dosing and two weeks after completion of multiple dosing. INBRX-101 concentrations were measured using a proprietary validated mass spectrometry assay specific to INBRX-101. BALF assessment results Rolled over from the Part 1 SAD2 had measurable INBRX-101 while drug was undetectable in INBRX-101 naïve patients (data not shown). Post-dose, INBRX-101 was present in each lung lobe of every patient for which a bronchoscopy was performed. The Phase 1 study data provide emerging evidence of a dose-dependent increase in INBRX-101 lung exposure. Each point represents the average INBRX-101 concentration measured across three lobes in an individual subject. Horizontal lines are the median values for each dose level.

13 INBRX-101 Modeled phase 2 dose of 120 mg/kg Q4W achieves AAT normal range Projected mean steady-state functional AAT levels pdAAT is only projected to achieve normal functional AAT levels for 2 – 2.5 days per weekly dose in AATD patients (9/28 days per month). INBRX-101 PK/PD modeling and simulation projections: 120 mg/kg Q4W is predicted to achieve and maintain steady-state functional AAT levels within the normal range. Troughs fully greater than 21.1 μM Average concentration of approximately 36 μM Overall exposure at steady-state (AUCs) twice that of pdAAT INBRX-101 pdAAT 36 μM mean of functional AAT normal range 11 μM historical putative threshold Fu nc tio na l A AT le ve ls (μ M ) 7 28 Time (days) Baseline: 0 40 80 60 20 2114

14 INBRX-101 Study INBRX101-01-201: ElevAATe INBRX-101 AATD registration-enabling trial Primary Endpoint: Mean change in avg fAAT concentration as measured by anti-neutrophil elastase capacity (ANEC) from baseline to average serum trough fAAT concentration at steady state (Ctrough,ss) Key Secondary Endpoints: INBRX-101 vs pdAAT: mean change in fAAT concentration from baseline to fAAT avg concentration at steady state (Cavg,ss), and % of days with fAAT above the lower limit of the normal range during steady-state dosing; Bronchoscopy sub-study of ~ 30 patients to run at designated sites Main Eligibility Criteria + Adult patients aged 18-80 with AATD and evidence of emphysema + AAT antigenic serum concentration <11 µM + Nonsmoker or former smoker + 5-week washout for those on augmentation therapy + Randomization stratified by baseline antigenic AAT & FEV1 (% predicted) Study INBRX101-01-202: ElevAATe-OLE (Open Label Extension) + Randomized, active controlled, double-blind + Head-to-head superiority study: INBRX-101 vs. pdAAT + 32-week treatment period + ~40 US, AUS, NZ sites N=36 INBRX-101 at 120 mg/kg Q4W & placebo on non-dosing weeks N=36 INBRX-101 at 120 mg/kg Q3W & placebo on non-dosing weeks N=18 pdAAT at approved dose of 60 mg/kg QW + Open label, long-term safety and tolerability study + Combination of naïve and rollover patients from ElevAATe + Minimum treatment duration of 3 years + ~40 US, AUS, NZ sites N=130 INBRX-101 120 mg/kg Q3W Initiated

15 INBRX-101 INBRX-101: AATD market opportunity ~100K ~100K ̴40K Upside market potential from continued increased rate of diagnosis and a focus on earlier prevention of lung loss Commercial viability of therapy requires abundant supply only available via INBRX-101 Sources: KOL interviews, Sandhaus chronic obstr pulm dis 2016; Barjaktarevic and Miravitlles BMC pulm med 2021 US prevalence Total treated US patients Market revenue potential TODAY FUTURE Severe* AATD cases *defined as <11 μM serum AAT levels US PI*ZZ & PI*SZ AATD market is growing at ~15% annually and projected to grow to $4B due to increased diagnosis. ̴8K–10K ~$1B ~$4B SZZZ

16 INBRX-101 Fred Hutch/Baxalta2 Ph1/2 (n=12) U of Michigan/CSL3 AAT +/- Prednisone Ph2 (n=40) Ef fic ac y ORR (%) at day 28 (per CIBMTR) 8/12 (67%) 26/40 (65%) CR (%) at day 28 4/12 (33%) 14/40 (35%) OS 6/12 alive 45% at 6 months Sa fe ty Grade 3+ AEs 0% 0% Most Frequent AEs “No clinical apparent toxicity in any patient” 2 d/c due to lack of efficacy “well tolerated with no infusion reactions or drug- related grade 3 to 4 toxicity” Incidence of Infection 0 13/40 (32.5%) Through 30 days Dosing 90 mg/kg loading dose followed by either 30 or 60 mg/kg every other day 60mg/kg per day every four days Ruxolitinib, Incyte1 (n=49) Ef fic ac y ORR (%) at day 28 (per CIBMTR) 28/49 (57%) CR (%) at day 28 15/49 (31%) OS 51% at 6 months Sa fe ty (n =7 1) Grade 3+ AEs 97.2% Most Frequent AEs + Anemia: 64% + Thrombocytopenia 62% + Neutropenia 48% Incidence of Infection 80% Dosing 5-10 mg twice daily National Comprehensive Cancer Network (NCCN) Ruxolitinib (category 1) Alemtuzumab Alpha-1 antitrypsin Anti-thymocyte globulin Basiliximab Calcineurin inhibitors Etanercept European Society for Blood and Marrow Transplantation (EBMT) Alemtuzumab Alpha-1 antitrypsin Basiliximab Cellular therapies Daclizumab Extracorporeal photopheresis Faecal microbiota transplantation Clinical data and established guidelines exist for AAT therapy in acute GvHD Active Phase 2/3 studies sponsored by CSL Behring The safety and efficacy of alpha-1 antitrypsin (AAT) for the prevention of graft-versus-host disease (GVHD) in patients receiving hematopoietic cell transplant (MODULAATE) (NCT03805789)3 Treatment of GVHD in hematopoietic stem cell transplant (HSCT) recipients using AAT plus corticosteroids (CS) compared with corticosteroids alone (NCT04167514)4 Sources: 1. https://www.Jakafi.Com/pdf/prescribing-information.Pdf, https://ashpublications.Org/blood/article/135/20/1739/452638/ruxolitinib-for-the-treatment-of-steroid 2. Response of steroid-refractory acute GVHD to a1-antitrypsin, marcondes et at, 2016. http://dx.Doi.Org/10.1016/j.Bbmt.2016.05.011 3. a1- antitrypsin infusion for treatment of steroid-resistant acute graft-versus-host disease, magenau et al, 2018. http://ashpublications.Org/blood/article-pdf/131/12/1372/1405639/blood815746.Pdf 4. https://clinicaltrials.Gov/ 5. listed in alphabetical order and not comprehensive of all consensus recommendations for steroid-refractory GVHD. Current Guidelines for aGVHD5 Existing clinical data for plasma-derived AAT therapies 2L (steroid resistant) aGVHD Existing clinical data for Jakafi: Current standard of care 2L (steroid resistant) acute GVHD (aGVHD) Unlike other existing options, INBRX-101 is expected to be combinable with other therapies due to its clean safety profile.

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

18 INBRX-109 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 INBRX-109 characteristics: Prevents cross- linking and higher order clustering IgG Fc Tetravalent Empirically designed to simultaneously engage four DR5 molecules Fc engineered to minimize effector function 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 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 Four DR5 sdAbs Empirically selected and engineered to avoid ADAs Tumor Cell Apoptosis Caspase C Programmed Cell Death C

19 INBRX-109 INBRX-109 is a potent inducer of extrinsic cell death via the DR5 pathway 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 INBRX-109 DR5 FADD Caspase activation 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. 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

20 INBRX-109 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 0.1 1 10 100 75 Impact of valency on cell death: 50 25 0 Valency EC 50 (p M ) 4 62 3 1000 100 10 1 0.1 5.78x 6.35x 94.2x Impact of valency on DR5-mediated cell death INBRX-109 tetravalent INBRX-109 tetravalent TRAIL trivalent Hexavalent DR5 hexavalent Hexavalent DR5 hexavalent Impact of valency on hepatotoxicity 100 10000.010.0010.0001 anti DR5 mAb bivalent 10-110-210-310-410-510-6 0 He pa to cy te v ia bi lit y (% ) % C el l d ea th Impact of valency on cell death: 10000 125 Test article (nM) Valency drives both DR5-induced tumor cell death and hepatocyte destruction

21 INBRX-109 INBRX-109: Phase 1 trial design Part 1 Part 2 Part 3 INBRX-109 single-agent dose escalation N=20 All comers 3+3 design evaluating doses of 0.3 to 30 mg/kg. INBRX-109 was well tolerated; MTD was not reached 3 mg/kg selected as RP2D INBRX 109 single-agent dose expansion Complete N=116 Ongoing Colorectal adenocarcinoma Synovial sarcoma Gastric adenocarcinoma IDH1/2-mutant conventional chondrosarcoma Malignant pleural mesothelioma Nonconventional chondrosarcoma Chondrosarcoma Solid tumors, BMI >30 N=20 N=10 N=10 N=12 N=20 N=12 N=20 N=12 Dose expansion with chemotherapy N=100 Ongoing Mesothelioma with carboplatin or cisplatin Ewing sarcoma 2-4L with irinotecan and temozolomide Mesothelioma with carboplatin and pemetrexed or cisplatin and pemetrexed Colorectal adenocarcinoma with FOLFIRI Pancreatic adenocarcinoma 2L with fluorouracil and irinotecan (mFOLFIRI) SDH-def solid tumors or GIST with temozolomide N=10 N=20 N=10 N=20 N=20 N=20 Study of INBRX-109 in patients with locally advanced or metastatic solid tumors, including sarcomas

22 INBRX-109 Encouraging mPFS and clinical responses observed in Chondrosarcoma patients treated with INBRX-109 Impact of valency on DR5-mediated cell death PFS by Kaplan-Meier analysis 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 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 + 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: 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. Overall median PFS: 7.6 months (range, 0.03-17.8 mo) vs. <4 months historically1-3

23 INBRX-109 INBRX-109 Phase 2 Registration Enabling Study Primary endpoint: Progression free survival Secondary endpoints: Overall survival, quality of life, overall response rate, duration of response, disease control rate, safety, etc. N=67*N=134* Patients Conventional chondrosarcoma, Grades 2 and 3, unresectable or metastatic Randomization stratified by line of therapy, Grade and IDH1/2 mutation status INBRX-109 for the treatment of unresectable and metastatic conventional chondrosarcoma + FDA fast track designation and orphan-drug designation + EMA orphan-drug designation Completion projected 2H 2024 INBRX-109 Placebo 3 mg/kg every three weeks 3 mg/kg every three weeks *Including interim analysis R 2:1 Ongoing Ongoing

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

25 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 INBRX-106 characteristics: 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 clustering Effector 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

26 INBRX-106 T cells NK cells Monocytes Dendritic cell Tumor T NK INBRX-106: mechanism of action T cell TCR MHC antigen Tumor cell TCR MHC antigen Tumor cell OX40 INBRX-106 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 bi-valent 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. c l s c l s onocytes ↑OX40 ↑ T cell

27 INBRX-106 Higher OX40 valency drives T cell activation and ability to overcome 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) 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 ~2-fold increase vs bi-valent and untreated Reversal of Treg Suppression2 CD8 T Cell Co-Stimulation1 CD4 T Cell Co-Stimulation1

28 INBRX-106 Valency drives OX40 agonism in CPI-resistant tumor models Syngeneic B16F10 Mouse Tumor Model *INBRX-106 mouse surrogate • 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*

29 INBRX-106 INBRX-106 study design Phase 1/2 study of single agent INBRX-106 and INBRX-106 in combination with pembrolizumab in patients with locally advanced or metastatic solid tumors Durable responses with anti-PD-1 in CPI-refractory patients across multiple tumor types Well-tolerated with mild or moderate immune- related toxicities Recently added single agent IO cohort to further elucidate contribution of benefit All-comers CPI r/r CPI naïve N=52-64 Basket Dose Regimen #1 Basket Dose Regimen #2 NSCLC PD-L1 or TMB high Basket Dose Regimen #3 INBRX-106 single-agent dose escalation Complete N=20 Dose expansion with pembrolizumab Complete N=21 Dose expansion with pembrolizumab Ongoing Basket PDL1+ NSCLC TMB or PDL1 high Basket PDL1 + NSCLC PDL1+ Basket, MMR-def/ MSI-high N=136 Part 1 Part 2 Part 3 Part 4 INBRX-106 single-agent dose escalation Ongoing Dose Regimen #1 Dose Regimen #2 Pembrolizumab Monotherapy Uveal melanoma Ongoing Ongoing Ongoing * Cohorts highlighted in green are actively recruiting

INBRX-105 tetravalent PD-L1 targeted 4-1BB agonist Localized 4-1BB agonist specific to PD-L1+ tissues Indiscriminate 4-1BB activation leads to a narrow therapeutic window limited by hepatotoxicity Previous generation therapy Goal: Restrict potent 4-1BB agonism to areas of high PD-L1 expression Inhibrx solution

31 INBRX-105 INBRX-105: localizing and potentiating the anti-cancer effects of the 4-1BB pathway FC Two 4-1BB sdAbs to conditionally agonize 4-1BB while allowing 4- 1BBL binding Two PD-L1 sdAbs to target and locally antagonize PD-1 interaction Fc engineered to minimize effector function Target T cell Tumor cell Stimulation T cells T cells NK cells T NK T INBRX-105 characteristics: Targeted to the tumor microenvironment in order to minimize hepatotoxicity Bispecific/ Conditional Agonist Localization Non- Competitive Binding INBRX-105 designed to boost anti-tumor T-cell activity in PD-L1 expressing tissues Designed to co-engage PD-L1 and 4-1BB in order to confer PD-L1 dependent 4-1BB agonism Complements natural ligand (4-1BBL) activity Smaller Size sdAb backbone limits molecule size (105 kDa) which may allow for better tumor penetration

32 INBRX-105 INBRX-105 mechanism of action The T-Cell Receptor (TCR) recognizes a tumor-associated antigen presented via MHC. This drives upregulation of 4-1BB on tumor reactive TILs to facilitate an immune response directed towards the tumor. By crosslinking 4-1BB at sites of high PD-L1 expression, INBRX-105 increases 4-1BB agonism to enhance T-cell survival, activation, and target killing localized to the tumor microenvironment. NK cells NK PD-L1 targeted 4-1BB agonism amplifies anti-tumor response and localizes T-cell activity Costimulation of 4-1BB leads to downstream activation on effector cells, including increased proliferation, cytotoxicity, memory generation and possible reversal of exhaustion. Tumor TT cells T cell TCRTCR MHCMHC antigenantigen ↑ T cell Tumor cell Tumor cell PD-L1PD-L1 4-1BB INBRX-105 ↑4-1BB

33 INBRX-105 INBRX-105 shows improved T cell modulation over PD-L1 and 4-1BB agents alone or in combination T Cell Co-stimulation2 MHC mismatch-induced TCR signal Co-stimulation with INBRX-105 following TCR engagement yields superior T cell cytokine production. INBRX-105 is more potent and induces enhanced cytokine production than PD-L1 blockade and 4-1BB agonism alone or in combination. * Analog of Urelumab was synthesized based on publicly disclosed sequences. 1 - PBMC stimulated with CEF (Cytomegalo-, Epstein-Barr- and Influenza-Virus) peptide mix, cytokine production measured by FluoroSpot. 2 - Mixed-lymphocyte reaction between cells from two MHC/HLA-mismatched donors, cytokine production measured by ELISA. IL -2 n g/ m L 0 10-3 Antibody (nM) 4 6 10 2 INBRX-105 Urelumab* Atezolizumab Urelumab + Atezolizumab No antibody 10-4 10-110-2 10110 102 8 IF N γ+ IF N α+ IL -2 + ce ll co un ts T Cell Co-stimulation1 Peptide-induced TCR signal 0 40 60 80 20 INBRX-105 Urelumab (4-1BB agonist) Atezolizumab (PDL1 Antagonist) Urelumab + Atezolizumab No antibody

34 INBRX-105 Localizing 4-1BB agonism to the PD-L1-rich tumor microenvironment leads to potent anti-tumor activity in mouse models MC38: PD-L1+ Tumor Model1 Dramatic increase in T cell frequency in the tumor microenvironment on Day 7 post dose of INBRX-105-a* INBRX-105-a* drives complete responses in PD-L1+ mouse tumor models (5/8 CRs) * Mouse reactive INBRX-105 surrogate. 1 - SD, IV C57BL/6, female. N=8/group. Enhanced T Cell Infiltration to TME Day 7 T ce ll fr eq ue nc y - f ol d ch an ge o ve r v eh ic le Blood Spleen Tumor 0 4 2 6 Tu m or v ol um e (m m 3 ) 5 15 Days post-dose 0 1500 2000 1000 500 INBRX-105 Vehicle 100

35 INBRX-105 INBRX-105 study design An open-Label, multicenter, dose-escalation, Phase 1/2 study of INBRX-105 and INBRX-105 in combination with pembrolizumab in patients with locally advanced or metastatic solid tumors CompleteSingle agent dose escalation N=32 Part 1 Part 2 NSCLC TPS >50% Cutaneous Melanoma or solid tumor HNSCC N=10 at 2nd dosing schedule N=22 at 1st dosing schedule2a N=32 N=30 Complete NSCLC TPS ≥ 50% HNSCC CPS ≥ 1%, MSI/TMB-high solid tumors HNSCC CPS ≥ 50% NSCLC TPS 1-49% N~ 50 Part 4 Dose escalation with pembrolizumab Part 3 Melanoma Single agent dose expansion Dose expansion with pembrolizumab All-comers CPI r/r CPI naïve 2b • NPC CPS ≥50% (n=24) • OPC and other HNSCC CPS ≥50% (n=24) Manageable early toxicity profile In preliminary data, single agent CRs and PRs observed in CPI r/r patients Complete Signals in Part 1/2a led to added single-agent expansion cohorts in HNSCC HNSCC CPS ≥50% (N=24-48) Ongoing Ongoing * Cohorts highlighted in green are actively recruiting

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