Inhibrx bone cancer trial: 5.52 vs. 2.66 months
An ozekibart Ewing sarcoma cohort reported a 64.5% objective response rate among 31 evaluable patients.
Sentiment and the balance of points
Rhea-AI Sentiment reads the wording of the document, how positive or negative its language is on a 1 to 5 scale. The balance of points shown with the takes weighs what the document actually discloses, so the two can disagree, for example when a trial that missed its main goal is described in upbeat language.
Form Type
8-K
Rhea-AI Filing Summary
Inhibrx Biosciences, Inc. (INBX) updated its corporate presentation on its clinical pipeline. In its randomized head and neck squamous cell carcinoma (HNSCC) study, INBRX-106 plus pembrolizumab had a confirmed objective response rate of 48.3% versus 26.5% with pembrolizumab alone. Six-month progression-free survival (PFS) was 72.4% versus 42.8%, and median PFS was 9.6 versus 4.9 months; median PFS remained maturing at the August 19, 2026 data cutoff.
Among HPV-positive patients, confirmed response rates were 80.0% (8/10) versus 33.3% (3/9), and six-month PFS was 90% versus 33%. An amendment adds 50 HPV-positive patients to Phase 2; the presentation describes a potential accelerated-approval path by end of 2028/early 2029. Any Grade ≥3 adverse events occurred in 58.1% versus 47.1%, and treatment discontinuations were 35.5% versus 14.7%.
Ozekibart met its primary endpoint in the chondrosarcoma registrational trial: median PFS was 5.52 versus 2.66 months (hazard ratio 0.479) and disease-control rate was 54.0% versus 27.5%; data cutoff September 30, 2025. In a Phase 1/2 colorectal cohort, 45 evaluable patients had a 20% objective response rate and 87% disease-control rate. The candidates discussed are investigational and not commercially available.
2 points · 1 major0 major · 1 point
How this balance works
Rhea-AI gives every point it takes from this document a weight. Minor counts 1, Moderate 3 and Major 9, so one Major point outweighs several Minor ones. The bar adds up the weights on each side, and when neither side holds more than 65% of the total the balance reads Mixed.
It reads the document as published, with the same rules for every company, and it does not look at what the market expected or at how the stock traded, so a point can be objectively good on a day the stock falls.
Rhea-AI Sentiment measures something else, the tone of the wording.
Positive
- Major pointOzekibart chondrosarcoma trial: primary endpoint met; median PFS 5.52 versus 2.66 months.
- Moderate pointINBRX-106 HNSCC response rate: 48.3% versus 26.5% in randomized study groups.
Negative
- Moderate pointHNSCC treatment discontinuations: 35.5% with combination versus 14.7% with pembrolizumab.
Insights
Analyzing...
8-K Event Classification
2 items: 7.01, 9.01
2 items
Item 7.01
Regulation FD Disclosure
Disclosure
Material non-public information disclosed under Regulation Fair Disclosure, often investor presentations or guidance.
Item 9.01
Financial Statements and Exhibits
Exhibits
Financial statements, pro forma financial information, or exhibit attachments filed with this report.
Key Figures
INBRX-106 confirmed objective response rate: 48.3% vs. 26.5%
INBRX-106 median PFS: 9.6 months vs. 4.9 months
INBRX-106 PFS at six months: 72.4% vs. 42.8%
+5 more
8 metrics
INBRX-106 confirmed objective response rate
48.3% vs. 26.5%
INBRX-106 plus pembrolizumab vs. pembrolizumab in randomized HNSCC study groups
INBRX-106 median PFS
9.6 months vs. 4.9 months
INBRX-106 plus pembrolizumab vs. pembrolizumab; median PFS remained maturing at August 19, 2026 data cutoff
INBRX-106 PFS at six months
72.4% vs. 42.8%
INBRX-106 plus pembrolizumab vs. pembrolizumab in HNSCC
HPV-positive confirmed response rate
80.0% vs. 33.3%
INBRX-106 plus pembrolizumab (8/10) vs. pembrolizumab (3/9)
Ozekibart median PFS
5.52 months vs. 2.66 months
Chondrosarcoma registrational trial, ozekibart vs. placebo; data cutoff September 30, 2025
Ozekibart hazard ratio
0.479
Primary endpoint in chondrosarcoma registrational trial
Ozekibart disease-control rate
54.0% vs. 27.5%
Chondrosarcoma registrational trial, ozekibart vs. placebo
HNSCC treatment discontinuation
35.5% vs. 14.7%
INBRX-106 plus pembrolizumab vs. pembrolizumab
Key Terms
progression-free survival, objective response rate, hazard ratio, accelerated approval, +1 more
5 terms
progression-free survival medical
"Median PFS was 5.52 versus 2.66 months"
Progression-free survival is the length of time during and after a treatment that a patient's disease does not get worse, measured from the start of treatment until the disease shows measurable signs of progression or the patient dies. Investors care because longer progression-free survival in clinical trials often signals that a drug is effective, improving chances of regulatory approval, market adoption, and revenue potential—think of it as a stopwatch showing how long a therapy can keep the illness at bay.
objective response rate medical
"Objective response rate was 20% as measured by RECISTv1.1"
The objective response rate (ORR) is the percentage of patients in a clinical trial whose tumors measurably shrink or disappear according to preset rules. Investors use it as a quick, objective signal of a drug’s ability to produce a clear treatment effect—like counting how many plants visibly respond after applying a new fertilizer—and higher ORR can improve odds of regulatory approval, commercial success, and company valuation.
hazard ratio medical
"HR, hazard ratio"
A hazard ratio is a way scientists compare the chance of something happening over time between two groups, like patients taking different medicines. If the ratio is high, it means one group is more likely to experience the event sooner or more often, which helps determine how effective a treatment is or how risky a situation might be.
accelerated approval regulatory
"Potential for accelerated approval"
Accelerated approval is a process that allows new medical treatments to be approved more quickly than usual if they address serious or life-threatening conditions and show promising early results. For investors, it signals that a treatment may reach the market sooner, potentially boosting a company's prospects, but it also involves some uncertainty since full evidence of effectiveness is still being gathered.
disease control rate medical
"Disease control rate (54% vs 27.5%)"
The disease control rate is the share of patients in a clinical trial whose cancer or condition either shrinks or stops getting worse for a specified period after treatment. Think of it like the percentage of people for whom a treatment hits pause or nudges back the problem rather than letting it progress; higher rates suggest the therapy can meaningfully limit disease, which matters to investors assessing a drug’s potential efficacy and commercial value.
FAQ
AI-generated questions and answers. How Rhea-AI works. Not financial advice.
What were INBX's ozekibart results in Ewing sarcoma?
In the Phase 1/2 irinotecan and temozolomide cohort, 20 of 31 evaluable patients had an objective response (64.5%), and 27 of 31 had disease control (87.1%). Thirty-nine patients had been dosed by the January 15, 2026 data cutoff.
What were INBX's ozekibart results with FOLFIRI in colorectal cancer?
In the Phase 1/2 colorectal adenocarcinoma cohort, ozekibart plus FOLFIRI had an objective response rate of 20%, a disease-control rate of 87%, and median PFS of 5.5 months. Forty-five patients were evaluable for response out of 50 in the cohort; the data cutoff was April 10, 2026.
AI-generated analysis. How Rhea-AI works. Not financial advice.
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
FORM 8-K
CURRENT REPORT
Pursuant to Section 13 or 15(d)
of the Securities Exchange Act of 1934
Date of Report (Date of earliest event reported): September 28, 2026
(Exact name of registrant as specified in its charter)
| (State or other jurisdiction of incorporation) | (Commission File Number) | (IRS Employer Identification No.) | ||||||||||||
(Address of Principal Executive Offices and Zip Code)
Registrant’s telephone number, including area code: (858 ) 795-4220
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:
Securities registered pursuant to Section 12(b) of the Act:
| Title of each class | Trading Symbol(s) | Name of each exchange on which registered | ||||||
Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).
Emerging growth company ☒
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☒
Item 7.01 Regulation FD Disclosure.
On September 28, 2026, Inhibrx Biosciences, Inc. (the “Company”) posted an updated copy of its corporate presentation to the “Investors” tab of its website at www.inhibrx.com. The presentation is attached to this Current Report on Form 8-K as Exhibit 99.1. The Company from time to time presents and/or distributes the presentation to the investment community during conferences and meetings to provide updates and summaries of its business. The Company undertakes no obligation to update, supplement, or amend the materials attached hereto as Exhibit 99.1.
The information in Item 7.01 of this Current Report on Form 8-K, including Exhibit 99.1 attached hereto, is intended to be furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any other filing under the Securities Act of 1933, as amended, or the Exchange Act, except as expressly set forth by specific reference in such filing.
Item 9.01. Financial Statements and Exhibits.
(d) Exhibits.
| Exhibit No. | Description | |||||||
| 99.1 | Corporate Presentation | |||||||
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document) | |||||||
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| Date: September 28, 2026 | ||||||||
| INHIBRX BIOSCIENCES, INC. | ||||||||
| By: | /s/ Kelly Deck | |||||||
| Name: | Kelly Deck | |||||||
| Title: | Chief Financial Officer | |||||||
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 $ Biosciences founded 2018 first IND 2020 IPO 2024 INBRX-101 acquisition by Sanofi 2010 >300 ozekibart (INBRX-109) Patients treated to date >175 INBRX-106 Patients treated to date Our mission: To discover & develop effective biologic treatments for people with life-threatening conditions Discovery Protein engineering Cell biology Translational research Chemistry Manufacturing and controls Clinical development and operations Commercial ~110 employees with an experienced leadership team 14.7M Common stock outstanding $219.5M Cash and cash equivalents 19.7M* Fully diluted outstanding Key financial highlights (as of 8/6/2026) * Includes 4.0M employee and BOD option reserve and approximately 1M pre-funded warrants and 0.2M warrants outstanding In-house expertise
4 INBRX-106 Data for randomized, first line HNSCC (INBRX-106/ Pembro vs. Pembro) HexAgon study Near term expected milestones Ozekibart (INBRX-109) Plan to meet with FDA to discuss 1L CRC registrational trial design and potential accelerated regulatory pathway for 4L CRC INBRX-106 Initiation of Phase 3 portion of HexAgon study Ozekibart (INBRX-109) Potential approval and first commercial launch of ozekibart for the treatment of metastatic or unresectable chondrosarcoma 2H 2026 1H 2027 2H 2027 Ozekibart (INBRX-109) Interim data from combination cohorts in CRC INBRX-106 Interim data from perioperative NSCLC study INBRX-106 Expansion of Phase 2 portion of HexAgon study INBRX-106 Data from expansion of Phase 2 HexAgon study
INBRX-106 Boosting PD-1 efficacy through next-generation hexavalent OX40 agonism
6 INBRX-106 • ORR: 80% vs 33% • CR Rate: 30% vs 0% • PFS Data: NR vs 4.6 months • PFS6 Rate: 90% vs 33% • Expansion of Phase 2 to include 50 additional HPV+ patients may serve as potential path to accelerated approval by end of ‘28/early ‘29. HPV+ HNSCC is an open $4B+ market INBRX-106 executive summary Combination with pembro demonstrates superiority to pembro mono in 1LR/M HNSCC Potentially practice-changing efficacy profile in HPV+ patients Large expansion opportunity in highly immunogenic tumors Potential for new paradigm of treatment with cancer vaccines INBRX-106 is the first clinically active OX40 agonist and T-cell costimulatory therapy • ORR: 48.3% vs 26.5% • Depth of Response • CR Rate: 13.8% vs 0% • PFS: 9.6 months vs 4.9 months • PFS6 Improvement: (72.4% vs. 42.8%) • These data are supported by superior t-cell proliferation (up to 15-fold increase) and activation (up to 4-fold increase) vs pembrolizumab alone • Bladder, NSCLC, Melanoma, MSI High/TMB High, TNBC present $50B+ commercial opportunity • Ongoing neoadjuvant lung cancer study serves as proof of concept for broad expandability with pembrolizumab across highly immunogenic tumors • Potential $50B+ market • HPV+ HNSCC data and over 20 years of academic research support the strong mechanistic rationale of INBRX-106 +cancer vaccines (OX40 agonism potency when foreign antigen is presented)
8 INBRX-106 T-cell activation critical steps: OX40 agonism enhances anti-tumor T cell activity in combo with PD-1 blockade (1) Croft. Ann Rev Immunol 2010. (2) Salek-Ardakani, Curr Imunol Rev 2006. (3) Weinberg, Immunol Rev 2011. (4) Piconese, J Exp Med 2008 T cell activation restored/enhanced Dual Immunotherapy: Releasing the Brakes and Stepping on the Gas Patients must have an immune response to their tumor(s) for signal 2 and check point inhibition to be impactful The ignition Signal 1: TCR tumor antigen recognition OX40 agonism enhances proliferation, survival and memory formation for tumor specific T-cells PD-1 signaling (in T-cells) activated via PD-L1 expressed in APCs and tumor cells dampens signal 1 and 2. PD-1 inhibition is necessary to remove this brake The accelerator Signal 2: OX40 T-cell co-stimulation The brake Check point inhibition Optimized T cell activation by OX40 agonism and PD-1 blockade Synergistic Tumor destruction via INBRX-106 and Pembro INBRX-106 is designed to: Supercharge the immune system against the tumors 1-4 Reverse immune suppression 1-4 Complement checkpoint inhibitors (anti-PD-1/PD-L1), enhancing activity
9 INBRX-106 0 500 1000 1500 2000 2500 0.01 1 100 10000 M ea n Va lu e Conc AB (ng/ml) Bivalent OX40 Agonist (Roche Analog) Hexavalent INBRX-106 Underwhelming activity among the 1st generation of bivalent OX40 therapeutics leads to INBRX-106 hexavalent OX40 JITC Providence Publication Hyper- clustering Hexavalent Simultaneously engages multiple OX40s to drive more potent clustering/signaling Receptor hyperclustering enables more efficient co-stimulation of OX40 (key for OX40 low expressing cells such as CD8 + T-cells) Bivalent OX40 Agonists Insufficient T-cell activation Suboptimal target engagement Bivalent IgG formats fail to drive high-order OX40 clustering required for co-stimulatory signaling Weak clustering impairs signaling and stalls proliferation Limitations of bivalent attempts Hexavalent OX40 Agonist Advantages of INBRX-106 format High-order OX40 clustering leads to stronger signal potency IN BR X- 10 6 Bi va le nt AF647 detection OverlayGFP high-order OX40 clustering low-order OX40 clustering *Holay et al. Journal for Immunotherapy of Cancer 2025 High-order OX40 clustering by INBRX-106 Low-order OX40 clustering by bivalent OX40 agonist Next Generation
10 INBRX-106 Head-to-head study serves as proof of concept, validating INBRX-106 Initial Study Design of HexAgon: Seamless Phase 2/3 study in 1L R/M HNSCC with PD-L1 CPS ≥20 Randomization stratified by: Disease status (locoregional advanced vs metastatic), HPV status (positive vs negative), ECOG PS (0 vs 1). In KEYNOTE-048, pembrolizumab achieved an ORR of 23.3% in the PD-L1 CPS ≥ 20 HNSCC population Clinicaltrials.gov (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 3, Double blind Survival Follow-up INBRX-106 + Pembro Pembro Co-primary endpoint: PFS and OS Secondary endpoints: ORR, DOR, CBR, TTCx, safety, PROs R 1:1 Primary Criteria: ORR Secondary Criteria: + DOR + CBR + PFS6m + Safety Phase 2, Open label INBRX-106 + Pembro Pembro Key inclusion criteria: R/M HNSCC PD-L1 CPS ≥20 HPV status confirmed No prior systemic Tx for R/M HNSCC R 1:1 Original Goals of HexAgon-HN Design - Contribution of components - Randomized add-on (106 + pembro vs pembro) cleanly isolates the benefit added by 106, aligns with regulatory expectations - Seamless Phase 2/3- fastest path to market
11 INBRX-106Baseline characteristics Baseline characteristics (randomized population)* 106 + Pembro N=33 Pembro N=35 Total N=68 Median age, y (min, max) 62.0 (35, 80) 66.0 (44, 89) 64.5 (35, 89) Age ≥65y, n (%) 13 (39.4) 21 (60.0) 34 (50.0) Male, n (%) 30 (90.9) 28 (80.0) 58 (85.3) ECOG PS 1, n (%) 17 (51.5) 18 (51.4) 35 (51.5) Distant metastatic disease, n (%) 18 (54.5) 21 (60.0) 39 (57.4) HPV positive, n (%) 10 (30.3) 9 (25.7) 19 (27.9) PD-L1 CPS ≥50, n (%) 24 (72.7) 23 (65.7) 47 (69.1) Prior systemic therapy, n (%)** 21 (63.6) 19 (54.3) 40 (58.8) Arms overall well-balanced *Median follow-up: 8.02 months (INBRX-106 + Pembrolizumab) vs. 6.31 months (Pembrolizumab). ** Systemic therapy received in the curative setting
12 INBRX-106 Most common TRAEs 106+Pembro All 106+Pembro ≥G3 Pembro All Pembro ≥G3 Rash maculo-papular 10 (32.3) 3 (9.7) 4 (11.8) 0 Rash 10 (32.3) 1 (3.2) 0 0 Fatigue 9 (29.0) 1 (3.2) 4 (11.8) 1 (2.9) Diarrhea 9 (29.0) 3 (9.7) 2 (5.9) 0 ALT increased 8 (25.8) 2 (6.5) 3 (8.8) 1 (2.9) AST increased 7 (22.6) 1 (3.2) 3 (8.8) 1 (2.9) Infusion related reactions 7 (22.6) 1 (3.2) 0 0 Safety & tolerability *Safety population = patients who at least received one dose of study treatment **Data comparison of HexAgon to KN-048 is not from head-to-head study; cross-trial comparisons are limited by differences in study designs, populations, regimens and follow-up The most frequent related adverse events are rash, fatigue, and diarrhea which were mostly grade 1 and 2 Overall safety — HexAgon-HN vs published KEYNOTE-048 pembrolizumab-monotherapy arm** Patients with ≥1, n (%) (safety population)* INBRX-106 + Pembro N=31 Pembro (HexAgon) N=34 KN-048 Pembro mono N=300 TEAE, any grade 31 (100) 29 (85.3) 290 (96.7) SAE, any grade 12 (38.7) 12 (35.3) 123 (41.0) Grade ≥3 AE, any/related 18 (58.1) / 15 (48.4) 16 (47.1) / 4 (11.8) 164 (55) Grade 5 AE 0 2 (5.9) 25 (8) Tx discontinuation 11 (35.5) 5 (14.7) 15 (5.0) Most common TRAEs in HexAgon-HN ≥20%
13 INBRX-106Discontinuation due to AE did not compromise antitumor activity in the combination arm *One additional patient discontinued due to AE in the combo arm but withdrew consent after discontinuation therefore not reflected in the graph. INBRX-106 + Pembrolizumab (n=10* discontinued for AE) Pembrolizumab alone (n=5 discontinued for AE) At least 9/10 (90%) Remained progression-free after discontinuing for an AE (INBRX-106 + pembrolizumab) 0/5 (0%) Remained progression-free after discontinuing for an AE (Pembrolizumab alone) Best response: ■ CR ■ PR ■ SD ★ Ongoing, progression-free ✕ Progressive disease/died ○ Censored Darker segment = time on treatment before AE-related discontinuation. Lighter segment = subsequent follow-up off treatment. ✕ ✕ ★ ✕ ★ ★ ★ ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20 ○ ○ ○ ✕ ✕ 0 2 4 6 8 10 12 14 16 18 20
14 INBRX-106INBRX-106+pembro drives up to 15-fold change in proliferation and up to 4-fold change in activation of T-cells vs. pembro mono Data cutoff date: April 2, 2026. RP2D (recommended phase 2 dose) for combination is 0.1 mpk of INBRX-106. Data is representative of Hexagon U.S. cohorts only (9 Pembro and 13 Combo patients). Data represented as Mean±SEM. 0 1 2 3 4 5 Pembro INBRX-106 +Pembro M ax F ol d Ch an ge fr om Ba se lin e – % o f A ct iv at ed M em or y Ce lls 0 5 10 15 20 25 Pembro INBRX-106 +Pembro M ax F ol d Ch an ge fr om Ba se lin e – % o f A ct iv at ed M em or y Ce lls 0 5 10 15 20 25 Pembro INBRX-106 +Pembro M ax F ol d Ch an ge fr om Ba se lin e – % o f A ct iv at ed M em or y Ce lls 0 1 2 3 4 5 Pembro INBRX-106 +Pembro M ax F ol d Ch an ge fr om Ba se lin e – % o f A ct iv at ed M em or y Ce lls HexAgon Phase 2 – 1L HNSCC • INBRX-106 is the key driver of T-cell activity in the combination group • INBRX-106 drives up to 15-fold change increase in proliferation and up to 4-fold change increase in activation of T-cells • Clear validation of INBRX-106 as a potent T-cell co-activator Proliferation Activation CD 8+ T c el ls CD 4+ T c el ls
15 INBRX-106Primary endpoint: Addition of INBRX-106 to pembro improves cORR Best % change in target lesion sum of diameters from baseline, RECIST v1.1. cORR = confirmed CR/PR on 2 consecutive occasions ≥4 weeks apart. Data from ongoing DB - CCOD 19 Aug 2026 * Evaluable population = Patients who have at least one post-baseline scan or have died or progressed INBRX-106 + Pembrolizumab Pembrolizumab ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ -100 -80 -60 -40 -20 0 20 40 ★ ★ ★ ★ ★ ★ ★ ★ -100 -80 -60 -40 -20 0 20 40 ■ CR ■ PR ■ SD ■ PD ★ Ongoing, progression-free 48.3% cORR — INBRX-106 + Pembro (n=29*) 95% CI 29.4–67.5 26.5% cORR — Pembro (n=34*) 95% CI 12.9–44.4 Δ +21.8 points Difference in cORR favoring INBRX-106 + Pembro
16 INBRX-106INBRX-106 improves overall durability & PFS across all patients *Median PFS still maturing; CCOD 19 Aug 2026 Bars show months of PFS follow-up, ranked longest to shortest, colored by best overall response. Data from ongoing DB - CCOD 19 Aug 2026. Note: Survival estimates are calculated using the Kaplan-Meier method. INBRX-106 + Pembrolizumab Pembrolizumab ■ CR ■ PR ■ SD ■ PD ★ Ongoing, progression-free 72.4% PFS at 6 months — INBRX-106 + Pembro 42.8% PFS at 6 months — Pembrolizumab ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20 ★ ★ ★ ★ ★ ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20 9.6 mo* Median PFS 4.9 mo Median PFS
17 INBRX-106Improved response & duration observed in HPV-negative patients *Median PFS still maturing; CCOD 19 Aug 2026. Note: Survival estimates are calculated using the Kaplan-Meier method. INBRX-106 + Pembrolizumab, HPV-negative Pembrolizumab, HPV-negative ■ CR ■ PR ■ SD ■ PD ★ Ongoing, progression-free 7.5 mo* Median PFS 5.1 mo Median PFS 63.2% PFS at 6 months, HPV-negative 31.6% cORR, HPV-negative (n=19) 46.8% PFS at 6 months, HPV-negative 24.0% cORR, HPV-negative (n=25) ★ ★ ★ ★ ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20 ★ ★ ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20
18 INBRX-106Increased benefit was observed in HPV+ patients Best % change in target lesion sum of diameters from baseline INBRX-106 + Pembrolizumab, HPV+ Pembrolizumab, HPV+ ■ CR ■ PR ■ SD ■ PD ★ Ongoing, progression-free 80.0% cORR, HPV+ INBRX-106 + pembro (n=10) 95% CI 44.4–97.5 33.3% cORR, HPV+ Pembrolizumab (n=9) 95% CI 7.5–70.1 Δ +46.7 points Difference in cORR, HPV+ INBRX-106+pembro vs. pembro mono 95% CI –2.7, 80.3 ★ ★ ★ ★ ★ ★ ★ ★ -110 -90 -70 -50 -30 -10 10 30 50 ★ ★ ★ -100 -80 -60 -40 -20 0 20 40
19 INBRX-106 ★ ★ ★ ★ ★ ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20 ★ ★ ★ 0 2 4 6 8 10 12 14 16 18 20 Enhanced durability & PFS observed in HPV+ patients *Median PFS still maturing; CCOD 19 Aug 2026. Bars show months of PFS follow-up, ranked longest to shortest, colored by best overall response. Data from ongoing DB - CCOD 19 Aug 2026. Note: Survival estimates are calculated using the Kaplan-Meier method. INBRX-106 + Pembrolizumab Pembrolizumab ■ CR ■ PR ■ SD ■ PD ★ Ongoing, progression-free 90% PFS at 6 months, HPV+ INBRX-106 + Pembro 33% PFS at 6 months, HPV+ Pembrolizumab Not reached* Median PFS 4.6 mo Median PFS
20 INBRX-106 Foreign viral antigen (E6/E7) driving a strong Signal 1, activated by OX40 co-stimulation on antigen-experienced T-cells Compelling Clinical Activity Attractive commercial opportunity: Potentially first dedicated HPV+ approval, differentiated from EGFR bispecifics (active mainly in HPV negative) Profound response-rate difference supports a potentially accelerated path to market The HPV+ signal is what the INBRX-106 mechanism predicts Opportunity to own HPV+ market Sound, mechanistic rationale High unmet need Potential for fast revenue realization Up to a 15-fold increase in peripheral CD8⁺/CD4⁺ T-cell proliferation and up to a 4-fold increase in activation (HexAgon-HN, interim Ph2) over ~2-fold pembrolizumab alone. 80% vs 33% cORR, HPV+ (106+Pembro vs Pembro) 90% vs 33% PFS6, HPV+ (106+Pembro vs Pembro) • HPV-driven tumors express viral E6/E7 neoantigens; these are foreign, high-quality targets that OX40 co- stimulation (INBRX-106's MoA) amplifies. • The enhanced results observed in HPV+ HNSCC are consistent with the expected underlying biology.
21 INBRX-106 The new study amendment adds an additional 50 HPV+ patients to the existing HexAgon design Expansion of Phase 2 HexAgon-HN with potential for an accelerated path to market in HPV+ Potential accelerated path by end of 2028/ early 2029 based on ORR as a surrogate likely to predict long-term clinical benefit (PFS & OS), and established precedent with petosemtamab and ficerafusp alfa Already part of the seamless design: serves as the confirmatory study for full approval Potential, based on preliminary signal magnitude in a serious, unmet-need indication Potential for breakthrough therapy designation Potential for accelerated approval Phase 3: confirmatory Opens the door to possibilities for accelerated development Phase 2 (additional 50 HPV+) Open label INBRX-106 + Pembro Pembro R 1:1 Phase 3 (n=TBD) Double blind, seamless INBRX-106 + Pembro Pembro R 1:1 Key inclusion criteria: R/M HNSCC HPV+ OPSCC PD-L1 CPS≥1
22 INBRX-106Rationale for expanding HPV+ enrollment to PD-L1 CPS≥1 Mandal R, et al. JCI Insight. 2016;1(17):e89829. Burtness B, et al. Lancet. 2019;394(10212):1915-1928. All Phase 2a patients both HPV+ and HPV-negative were enrolled at PD-L1 CPS≥20 • PD-L1 expression was therefore held constant across the two subgroups and despite this the increase in response rates with the combination was much greater in the HPV+ • If CPS>20 was the driver you would see similar increase in ORR independently of HPV status • If INBRX-106's HPV+ benefit is driven by antigen availability rather than PD-L1 level, lowering to CPS>1 should not impact the ability of OX-40 to amplify the tumor response Pembrolizumab alone + INBRX-106 HPV+ cORR 33.3% (3/9) 80.0% (8/10) HPV-negative cORR 24.0% (6/25) 31.6% (6/19) The Phase 2b expansion: HPV+ OPSCC patients across CPS≥1, stratified by CPS (1–19 vs ≥20) is designed to test this directly and prospectively. Validation This data reflects the distinct immunogenic biology of HPV-driven tumors, (viral E6/E7 oncoproteins provide a foreign), recognizable antigen source for OX40 to amplify rather than a PD-1-pathway-sensitivity effect. Working hypothesis
23 INBRX-106 ~$1B ~$2B ~$1B Set to pursue a breakthrough pathway in 1L R/M HPV+ CPS ≥1 HNSCC Source: SEER Explorer, CDC, Clarivate Disease Landscape Report ~$4B+ U.S. market opportunity including stage I-III setting 2.6% Rapidly Growing Market US Epidemiology Estimates Valuation Drivers US Sales Potential High morbidities in current therapies Clinicians actively seeking de-escalation therapy in HPV+. Significant radiation- and surgery-related morbidities — e.g., impaired speech, feeding tube High share; higher systemic usage Significant unmet need for a therapy specifically studied in the HPV+ population; where current EGFR bi-specifics do not perform well Premium pricing Ground-breaking results and limited patient population would provide opportunity for premium pricing. Premium priced therapies currently on guidelines Long duration High response rate, and deep and durable responses on INBRX-106 point to longer duration on therapy ~30,000 2029 US Incidence (De Novo Stage I-IV + Recurrent) HPV+ HNSCC Patients in the US ~8,000 Stage I-III Surgical ~16,000 Stage I-III Non- Surgical ~6,000 1L R/M US Annual Growth in HPV+
24 INBRX-106 INBRX-106: multiple attractive expansion opportunities Source: 1. Evaluate estimates for PD-1s projected to 2031 based on 2025-2027 growth rates (market size independent of biosimilar entry). 2. Virally antigen estimated based at 3x HPV based on topline epidemiology from CDC or IARC (de Martel) projected WW. 3. Company estimate, full impact of V940 data release 8/19/26 not yet propagated through reports. Highly Immunogenic Tumors • NSCLC • Melanoma • Renal Cell Carcinoma • TNBC • Bladder • MSI-H / dMMR • TMB-High Virally Antigen-Driven • HPV+ H&N • HPV+ beyond H&N (e.g., Anus/ Rectum, Cervix, Vagina, Vulva, Penis) • Non-HPV, commonly reported virally- linked cancers: EBV, HBV, HCB, HTL1-1, HHV-8 Individualized Neoantigen Cancer Vaccines Major Ph 2/3 programs: • Moderna/Merck: (V940): Melanoma, NMIBC, NSCLC • BioNTech/Genentech (Autogene Cevumeran): CRC, PDAC $50 B+1 $15 B+2 $50 B+3 Ongoing clinical trial in peri-operative NSCLC and IST in peri-operative TNBC serves as fast proof of concept for broad expandability to other immunogenic tumors Seek potential combinations with individualized neoantigen cancer vaccines Expand Phase 2 portion of HexAgon-HN trial to increase HPV+ patients for potential accelerated approval Ongoing studies & development plan WW Market Opportunity: Highest impact expected in early stage disease Increased opportunity for OX40 agonism due to increased ongoing antigen-driven T-Cell stimulation
25 INBRX-106 Highly immunogenic tumors, peri-operative NSCLC expansion: pCR is a fast, validated readout of long-term benefit 1. Wakelee et al., KEYNOTE-671, N Engl J Med 2023 • Pathologic complete response (pCR) at surgery: • Available in months, not years • Highly correlated with improved survival and can generate a second, independent proof-of-activity signal well ahead of any survival endpoint • pCR in peri-operative NSCLC opens a multibillion-dollar market opportunity and will serve as proof of concept for expandability to other highly immunogenic tumors, broadening the platform thesis beyond HNSCC KEYNOTE-671 0.58 Event-free survival HR (95% CI 0.46–0.72)¹ 18.1% Pathologic complete response Pembro+chemo Neoadjuvant study – Ongoing Ph1/2 study expected to read-out by mid-2027 Stage II–IIIB NSCLC, ECOG 0–1, surgical candidates Participants (N~40) Neoadjuvant (4 cycles) Adjuvant (13 cycles) Surgery Primary endpoints + pCR + Safety Platin doublet + pembro + INBRX-106 Pembro + INBRX-106
26 INBRX-106 INBRX-106 HPV+ ORR data and 20+ years of academic research1 support synergy of OX40 agonism and potential vaccine effectiveness 1. Appendix includes a curated set of 18 high impact publications • Extensive preclinical evidence: OX40 agonism enhances vaccine efficacy/anti-tumor activity • INBRX-106 HPV⁺ HNSCC high ORR validates that OX40 co-stimulation amplifies immunity response to APC-presented antigen • mRNA vaccine recreates HPV+ like tumor antigenicity by design INBRX-106 Hexavalent agonist antibody ± anti-PD-1 checkpoint release + Tfh-B cell help Germinal Center Stronger CD8 effector-memory responses Stronger CD4 Th1 / effector-memory responses Improved antibody response Vaccines provide tumor-driven antigens that T-Cells recognize Anti-Tumor OX40 ⁺T-cell is highly responsive to OX40 agonism OX40 T-cell co- activation Enhanced anti- tumor activity Signal 1 Signal 2
27 INBRX-106 Combinability may enable INBRX-106 to capitalize on recent breakthrough of individualized neoantigen cancer vaccines IPV* Clinical validation INBRX-106 POC validation Individualized vaccine Primes neoantigen-specific T cells Inhibrx-106 OX40 agonism Amplifies T-cell antigenic response expansion and durability Strategic opportunity Moderna's V940 (intismeran autogene) + pembrolizumab has established clinical validation in adjuvant melanoma In-patient T-cell Co-stim: CD8+ prolif. (fold ↑) Phase 2 0.51 RFS hazard ratio 0.38 DMFS hazard ratio • Favorable exploratory OS trend • Phase 3 positive top-line readout created $25B+ market value overnight • Chronic MHC-presented HPV antigen sustains an OX40+ T-cell phenotype a personalized vaccine can recreate • Strong Preclinical Evidence: OX40 agonism-vaccine synergy. Antigen specific T-cell expansion, survival, memory, humoral response Clinical PoC: HPV+ OPC — ORR INBRX-106 + pembrolizumab 15× Pembrolizumab 2× ~80% 33% INBRX-106 + pembrolizumab Pembrolizumab Potential best-in-class outcomes *IPV-Individualized Patient Vaccine
28 INBRX-106 • ORR: 80% vs 33% • CR Rate: 30% vs 0% • PFS Data: NR vs 4.6 months • PFS6 Rate: 90% vs 33% • Expansion of Phase 2 to include 50 additional HPV+ patients may serve as potential path to accelerated approval by end of ‘28/early ‘29. HPV+ HNSCC is an open $4B+ market INBRX-106 conclusion Combination with pembro demonstrates superiority to pembro mono in 1LR/M HNSCC Potentially practice-changing efficacy profile in HPV+ patients Large expansion opportunity in highly immunogenic tumors Potential for new paradigm of treatment with cancer vaccines INBRX-106 is the first clinically active OX40 agonist and T-cell costimulatory therapy • ORR: 48.3% vs 26.5% • Depth of Response • CR Rate: 13.8% vs 0% • PFS: 9.6 months vs 4.9 months • PFS6 Improvement: (72.4% vs. 42.8%) • These data are supported by superior t-cell proliferation (up to 15-fold increase) and activation (up to 4-fold increase) vs pembrolizumab alone • Bladder, NSCLC, Melanoma, MSI High/TMB High, TNBC present $50B+ commercial opportunity • Ongoing neoadjuvant lung cancer study serves as proof of concept for broad expandability with pembrolizumab across highly immunogenic tumors • Potential $50B+ market • HPV+ HNSCC data and over 20 years of academic research support the strong mechanistic rationale of INBRX-106 +cancer vaccines (OX40 agonism potency when foreign antigen is presented)
P R OP R IE TAR Y AN D C ON FID E N TI A L; N OT FOR D IS TR IB U TION 106 Appendix
30 INBRX-106 18 selected preclinical studies spanning protein, DNA/viral-vector, whole-cell and RNA vaccine platforms, plus first-in-human proof of biology OX40 agonism enhances vaccine efficacy: broadly supported in scientific literature for 20+ years Foundational mechanism & platforms Therapeutic cancer vaccines Cancer (cont.) & RNA-era platforms HUMAN PROOF OF BIOLOGY Curti / Weinberg 2013, Cancer Research (first-in-human OX40 agonist study): patients receiving reporter-antigen immunizations showed increased T-cell and B-cell responses to the vaccine antigens — direct clinical evidence that pharmacologic OX40 agonism augments vaccine responses. Gramaglia 2001 · J Immunol · PMID 11739496 Soluble antigen vaccine: ~10× antibody titers and durable CD4 memory. Laderach 2004 · Immunology · PMID 15270726 DNA prime / poxvirus boost: higher CD4 responses; +4-1BB further raises CD8. Ruby 2007 · Eur J Immunol · PMID 17183611 Greater CD8 memory survival and recall — durability, not just expansion. Redmond 2007 · J Immunol · PMID 18025166 Restores CD8 effector function and granzyme B after antigen priming. Sanchez 2012 · PMID 22186790 Adenovirus vaccine + OX40: improved protection against viral challenge. Welten 2017 · PMID 28265272 Peptide booster vs MCMV: stronger CD4/CD8 responses; lower viral titers. 1 2 3 4 5 6 Murata 2006 · J Immunol · PMID 16393983 GM-CSF whole-cell vaccine: overcomes CD8 tolerance to endogenous tumor antigen. Murphy 2012 · Clin Cancer Res · PMID 22781551 Glioma lysate + Fc-OX40L: ~50–100% cures with rechallenge protection. Murphy / Fecci 2013 · PMID 24293627 Same regimen; regression dependent on CD4 T, NK and B cells. Linch 2016 · PMID 26729864 HER2 DC-targeted vaccine + αOX40/αCTLA-4: reverses anergy, improves survival. Jahan 2018 · Neuro-Oncology · PMID 29016879 GVAX + αOX40 in glioma: median survival 22 → 36 days; better CD8:Treg balance. Jahan 2019 · PMID 31069135 GVAX + αPD-1 + αOX40: long-term survival in all treated mice. 7 8 9 10 11 12 Peng 2019 · Clin Cancer Res · PMID 31371342 gp100 peptide / DC vaccination: greater antigen- specific CD8 expansion and memory. Du 2022 · J Cancer Res Clin Oncol · PMID 35748951 Whole-cell vaccine + CpG/αOX40/cGAMP: slower growth, more intratumoral T cells. Sun 2023 · J Transl Med · PMID 37700338 In-situ vaccine (radiation + CpG + OX40): local and abscopal tumor control. Li 2020 · Vaccines · PMID 32210183 Rabies vector expressing OX40L: more Tfh and germinal-center B cells. Duhen 2022 · Front Immunol · PMID 36238275 SARS-CoV-2 protein and saRNA vaccines: higher, longer-lasting antibody and CD4/CD8 responses. Lu 2025 · JCI Insight · PMID 40178907 Zika saRNA + OX40/4-1BB: immunity extended to day 84; lower viral load on delayed challenge. 13 14 15 16 17 18 19
Ozekibart (INBRX-109) Selectively inducing apoptosis in tumor cells through tetravalent DR5 agonism
32 INBRX-109 Unprecedented data in chondrosarcoma Ozekibart (INBRX-109) chondrosarcoma registrational trial results Primary endpoint met: • HR= 0.479; (95% CI: 0.33, 0.68); P<0.0001 (52% reduction in the risk of disease progression or death) • More than doubling median PFS to 5.52 months compared to 2.66 months for placebo • Ozekibart’s benefit was consistent across all pre-specified subgroups Secondary endpoint: • Disease control rate (54% vs 27.5%) Patients: Conventional chondrosarcoma, Grades 2 and 3, unresectable or metastatic Ozekibart (INBRX-109) Placebo Regulatory momentum Orphan designations (FDA & EMA) and Fast track (FDA) Improved disease control rate 54% vs 27.5% Median PFS more than doubled 5.52 months vs 2.66 months 52% reduction in progression or death HR 0.479; P < 0.0001 Every three weeks N=137 Every three weeks N=69 R 2:1 Randomization stratified by line of therapy, Grade and IDH1/2 mutation status
33 INBRX-109 Primary endpoint: progression-free survival by CIRR (a) Per RECIST, v1.1. (b) CI was calculated using Clopper-Pearson exact method, which does not take stratification factors into consideration. (c) A Cochran-Mantel-Haenszel test stratified by randomization stratification factors to adjust for possible confounding effects of the stratification factors was used to calculate the P value. (d) The BOR was NE in 7 patients who received ozekibart and 2 who received placebo due to no available postbaseline scans. (e) The study inclusion criteria of measurable disease according to RECIST (and progression within 6 months) was evaluated using the investigator assessment of tumor images only; confirmation of the investigator’s assessment by the central reader was not required. Due to differences in lesion selection and/or lesion measurements upon central review, 4 patients did not have measurable target lesions per central reader. These patients were followed for disease progression based on non- target disease; thus, the target lesion response was considered NE by the central reader, and only the non-CR/non-PD designation could be selected for SD in these 4 patients. Data cutoff date: September 30, 2025. Crosses indicate censored patients. Data from the double-blind period of the study are presented. CIRR, central independent radiology review; HR, hazard ratio; mPFS, median PFS; PFS, progression-free survival. Ozekibart significantly prolonged mPFS vs placebo and led to a 52% reduction in the risk of disease progression or death Time, months 3 months 6 months 12 months 0 5 10 15 20 25 30 35 0.0 0.2 0.4 0.6 0.8 1.0 Pr ob ab ili ty o f P FS Placebo 40.9% 16.9% 9.7% Ozekibart 70.1% 21.7% 47.2% No. at risk: Ozekibart 137 56 24 11 4 2 2 0 Placebo 69 16 2 1 0 0 0 0 Ozekibart N=137 Placebo N=69 Primary Efficacy Endpoint Events / Censored, n (%) 94 (68.6) / 43 (31.4) 55 (79.7) / 14 (20.3) mPFS, months 5.52 2.66 Stratified HR (95.02% CI) 0.479 (0.335–0.684) Log-rank P value <0.0001 Disease Control Rate by CIRR DCR, n (%)d 74 (54.0) 19 (27.5) 95% CIe 45.3–62.6 17.5–39.6 Percentage point difference (95% CI) 25.9 (11.7–38.3) P < .001f
34 INBRX-109 IDH mutation status Wild type Mutant Prior treatment Yes No Histologic grade at entry 2 3 Disease status at entry Metastatic Nonmetastatic unresectable Region US Outside of US Age <65 years ≥65 years Sex Male Female Race White Other BMI <30 kg/m2 ≥30 kg/m2 ECOG PS 0 1 Progression-free survival by CIRR: subgroup analyses Data cutoff date: September 30, 2025. a N values represent the number of patients with available data for each parameter. BMI, body mass index; CIRR, central independent radiology review; ECOG PS, Eastern Cooperative Oncology Group performance status; HR, hazard ratio; CI, confidence interval; IDH, isocitrate dehydrogenase; mPFS, median progression-free survival. PFS benefit was consistent across key prespecified subgroups, including IDH mutation status & prior therapy favors Ozekibart 0 1 2 3 Ozekibart Placebo Events, n/Na mPFS, mo Events, n/Na mPFS, mo HR (95% CI) 65/93 5.5 38/47 2.7 0.493 (0.324-0.750) 29/44 5.5 17/22 2.3 0.442 (0.224-0.871) 38/58 5.3 21/28 2.7 0.546 (0.307-0.971) 56/79 7.4 34/41 2.7 0.441 (0.280-0.693) 65/96 7.2 36/48 2.7 0.485 (0.316-0.747) 29/41 5.3 19/21 1.4 0.464 (0.246-0.875) 87/122 5.5 47/56 1.5 0.424 (0.288-0.624) 7/15 5.5 8/13 5.4 0.675 (0.199-2.286) 42/65 7.6 24/32 2.0 0.517 (0.288-0.928) 52/72 4.3 31/37 2.7 0.524 (0.316-0.870) 68/104 7.4 40/52 2.6 0.398 (0.257-0.615) 26/33 5.3 15/17 2.7 0.476 (0.217-1.047) 69/96 5.4 37/42 2.7 0.545 (0.353-0.840) 25/41 7.6 18/27 2.6 0.270 (0.123-0.592) 75/114 5.5 38/47 2.7 0.546 (0.358-0.835) 19/23 7.4 17/22 2.7 0.348 (0.148-0.818) 76/112 5.6 43/53 2.6 0.499 (0.333-0.747) 18/25 4.3 12/16 2.7 0.472 (0.156-1.423) 33/51 7.6 23/29 2.7 0.404 (0.215-0.758) 60/85 5.5 32/39 2.7 0.515 (0.319-0.830)
35 INBRX-109 Double-blind period Ozekibart N=136 Placebo N=67 Patients with ≥1 AE (including unrelated AEs), n (%) 129 (94.9) 62 (92.5) Grade ≥3 53 (39.0) 17 (25.4) SAE 38 (27.9) 12 (17.9) HAE 21 (15.4) 9 (13.4) Resulting in death 5 (3.7) 1 (1.5) Patients with ≥1 treatment-related AE, n (%) 77 (56.6) 32 (47.8) Grade ≥3 14 (10.3) 1 (1.5) SAE 8 (5.9) 0 HAE 16 (11.8) 3 (4.5) Leading to interruption of study drug 8 (5.9) 2 (3.0) Leading to discontinuation of study drug 4 (2.9) 0 Resulting in death 1 (0.7) 0 Overall safety data Data cutoff date: September 30, 2025. AE, adverse event; HAE, hepatic adverse event; SAE, serious adverse event. HAEs included alanine aminotransferase increased, aspartate aminotransferase increased, bile duct stone, bilirubin conjugated increased, blood alkaline phosphatase increased, blood bilirubin increased, feces discolored, gamma-glutamyl transferase increased, hepatic failure, hyperbilirubinemia, hypertransaminasemia, and liver disorder.
36 INBRX-109 Key inclusion criteria CRC 3-4L with FOLFIRI Initial data from Phase 1/2 colorectal adenocarcinoma in combination with FOLFIRI Data cutoff: April 10, 2026. Safety: well-tolerated with the most common treatment-related adverse events to include diarrhea, fatigue, and nausea with the majority being low-grade and consistent with the known safety profile of FOLFIRI. 68% of patients presented with liver metastases prior to treatment and no significant liver toxicity issues were observed in these patients. ~70% are 4th line & ~30% are 3rd line ~80% have received prior IRI-containing regiment Disease control rate was 87% as measured by RECISTv1.1 87% Objective response rate was 20% as measured by RECISTv1.120% Median progression free survival was 5.5 months5.5 42% of patients remained progression-free at the 6-month mark42% • LA/M, unresectable, R/R colorectal adenocarcinoma • Aged 18 to <85 years • 2-3 prior lines of systemic therapy Ozekibart 3 mg/kg + FOLFIRI (FU, 2400 mg/m2; leucovorin, 400 mg/m2; IRI, 180 mg/m2) 45 patients evaluable for response N=50
37 INBRX-109 Data cutoff: April 10, 2026. CR, complete response; PD, progressive disease; PR, partial response; SD, stable disease; NA, censored. Phase 1/2 colorectal adenocarcinoma in combination with FOLFIRI Months CR PR SD PR SD PR SD SD SD SD PR SD SD SD SD SD PR SD SD SD SD SD PR SD PR SD SD SD SD SD SD SD SD SD SD SD SD PR SD PD PD PD PD PD PD NA NA NA NA NA 0 1 2 3 4 5 7 8 9 10 11 13 14 15 16 17 19 206 12 18 Individual patient time on treatment shows sustained disease control in heavily pre-treated patients 2 lines of prior therapy 3 or more lines of prior therapy Durable responder Response start Response end Progressive disease Patient died Patient censored Ongoing progression free patient Prior Treatment Status:
38 INBRX-109Phase 1/2 colorectal adenocarcinoma in combination with FOLFIRI Data cutoff: April 10, 2026. PD, progressive disease; PR, partial response; a Per RECIST v1.1 20% target lesion growth indicates progressive disease. b Per RECIST v1.1 30% shrinkage of target lesions indicates a partial response. contingent on the status of the non-target lesions and the presence of new lesions. 25 -3 -3 -6 -14 -16 -17 -25 -28 -31 -53 -54 32 26 22 17 11 5 5 -3 -3 -4 -7 -10 -11 -15 -16 -21 -21 -22 -23 -31 -31 -34 -37 -44 -76 -100 PDa PRb -100 -80 -60 -40 -20 0 20 40 Ch an ge fr om B as el in e, % 2 lines of prior therapy 3 or more lines of prior therapy Benchmarks ORR (%) Lonsurf + bev (SUNLIGHT, 2023) 6.1 regorafenib (CORRECT, 2013) 1.0 fruquintinib (FRESCO-2, 2023) 1.5 Prior Treatment Status: 20% Objective Response Rate
39 CRC expansion cohorts: open and enrolling COMBINATION (n=270) Colorectal adenocarcinoma Age ≥18 to <85 years Part 3: dose expansion Ozekibart + chemotherapy ONGOING C4 CURRENTLY ENROLLING Colorectal adenocarcinoma (LA/M, unresectable, R/R) • Patients with no prior exposure to FTD/TPI • 2-3 prior lines of systemic therapy Regimen: Ozekibart + FTD/TPI + bevacizumab C4f (n≈30) Colorectal adenocarcinoma (LA/M, unresectable, R/R) • Patients with no prior exposure to IRI-based regimen • 1 prior line of systemic therapy Regimen: Ozekibart + FOLFIRI + bevacizumab C4e (n≈30) Cohort N Regimen Population Rationale C4e 30 109+ FOLFIRI 2L+, No prior IRI-containing regimen Provide safety data in combination with Bev and additional activity data on a IRI naïve populations C4f 30 109 + Lonsurf + Bev 3L+ no prior exposure to Lonsurf Efficacy signal w 3-4L with Lonsurf+Bev (opening opportunity for expanding to Ph3 in late setting) 2L, second line; 3L, third line; FOLFIRI, fluorouracil, leucovorin, and irinotecan; FTD/TPI, trifluridine-tipiracil; IRI, irinotecan; LA/M, locally advanced/metastatic; R/R, relapsed or refractory; TMZ, temozolomide.
40 INBRX-109Ongoing phase 1/2 trial in Ewing sarcoma in combination with IRI/TMZ Expected outcomes with current SoC Treatment Study Type ORR (%) PFS (months) Irinotecan + Temozolomide Phase 2 / single-arm ~15–30 3–4 HD Ifosfamide Phase 2 / rEECur ~20–25 5.7 Key inclusion criteria EWS 2-3L with IRI/TMZ • LA/M, unresectable, R/R EWS • Aged ≥12 to <85 years • EWSR1-FLI1, -ERG or -FEV rearrangement • 1-2 prior lines of chemotherapy in metastatic setting • Prior IRI + TMZ allowed Ozekibart 3 mg/kg + IRI 50 mg/m2/day + TMZ 100 mg/m2/day N=50
41 INBRX-109 PD PR -100 -80 -60 -40 -20 0 20 40 60 80 100 Ch an ge fr om B as el in e, % Yes Updated data from expansion cohort: Ewing sarcoma in combination with IRI/TMZ Data cutoff: January 15, 2026, as presented at the ESMO Sarcoma and Rare Cancers Annual Congress. PD, progressive disease; PR, partial response; ORR, objective response rate; DCR, disease control rate. Safety: well-tolerated with the most common adverse events were diarrhea, nausea, anemia, and fatigue, all consistent with the known safety profile of IRI/TMZ. Recruitment ongoing 39 patients dosed with 31 patients currently evaluable for response: Prior IRI/TMZ Treatment (N=31) 87.1% Disease control rate was 87.1%, or 27 out of 31 patients, as measured by RECISTv1.1 64.5% Objective response rate was 64.5%, or 20 out of 31 patients, as measured by RECISTv1.1
42 INBRX-109Sarcomas offer a blockbuster $1B+ revenue opportunity; CRC offers a franchise-defining opportunity Epidemiology based on SEER, SEER Explorer, and CancerMPact US Epidemiology Estimates Sarcomas CRC 1L Conventional Chondrosarcoma 2L+ Ewing Sarcoma 1L 3L Unresectable/metastatic 200 – 400 Newly diagnosed 2,000 – 3,000 Prevalent at launch 200 – 400 Newly diagnosed 2,000 – 3,000 Prevalent at launch 75,000 20,000 Valuation Drivers • High share and no competition • Ultra rare oncology pricing • Long duration in cCS due to lack of available 2L options • High share with limited competition in all-comers population • Premium oncology pricing • Very long 1L duration due to maintenance post chemo WW Product Sales Potential $500M + $500M + $10B+ $4.5B+
P R OP R IE TAR Y AN D C ON FID E N TI A L; N OT FOR D IS TR IB U TION 109 Appendix
44 INBRX-109 0 7 14 21 28 35 42 49 0 20 40 60 80 100 0 20 40 60 80 100 0 7 14 21 28 35 42 49 56 63 70 77 84 0 20 40 60 80 100 y Ozekibart exhibits anti-tumor activity in GBM models as monotherapy and in combination with TMZ *In collaboration with Jann Sarkaria, M.D., Mayo Clinic • In all tested intracranial PDX tumor mouse models, ozekibart monotherapy significantly enhanced survival • In 2 of 3 PDX models, combination treatment with ozekibart and TMZ led to a greater survival benefit than TMZ alone • Combination treatment with ozekibart and temozolomide (TMZ) induced greater in vitro cell death than TMZ alone for a majority of GBM cell lines tested (n=31) • In the intracranial U-87 MG tumor mouse model, combination treatment demonstrated superior tumor control and enhanced survival compared to TMZ alone Intracranial GBM44 Survival analysis Intracranial GBM38 Survival analysis Intracranial GBM39 Survival analysis *p = 0.002, INBRX-109 vs vehicle ** p – 0.004, combo vs TMZ *p = 0.03, INBRX-109 vs vehicle ** p – 0.01, combo vs TMZ *p = 0.009, INBRX-109 vs vehicle Pr ob ab ili ty o f S ur vi va l Pr ob ab ili ty o f S ur vi va l Pr ob ab ili ty o f S ur vi va l Study Day Study DayStudy Day Median Survival (d) Treatment GBM38 GBM39 GBM44 Vehicle 17 22 42 INBRX-109 25 33 58 TMZ 33 n.d. 39 Combo 42 n.d. 74 0 2 4 6 8 10 12 7.4 1.1 0 7 14 21 28 35 42 49 56 63 70 77 0 20 40 60 80 100 Vehicle INBRX-1 TMZ INBRX-1 -25 0 25 50 75 100 0 20 40 60 80 [TMZ] (∝M) In vitro cytotoxicity GBM cell lines In vitro cytotoxicity U-87 MG INBRX-109 only (1nM) Intracranial U-87 MG Survival analysis Intracranial U-87 MG Survival analysis % c el l d ea th % c el l d ea th Pr ob ab ili ty o f S ur vi va l Fo ld c ha ng e fr om b as el in e Study Day TMZ + 1 nM INBRX-109 TMZ INBRX-109 Vehicle INBRX-109 + TMZ TMZ Human GBM cell line models Human GBM patient-derived xenograft (PDX) models*
Investor Relations: KELLY DECK, CPA CFO 11025 N. Torrey Pines Road Suite 140 La Jolla, CA 92037 858.795.4260 ir@inhibrx.com