Exhibit 99.1

Building a Universal - RAS Franchise Nasdaq: IMRX APRIL 2023 Investor Presentation

 

2023 Corporate Presentation 2 This presentation contains forward - looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 . All statements contained in this presentation that do not relate to matters of historical fact should be considered forward - looking statements, including, without limitation, statements regarding the Company's cash, cash equivalents and marketable securities as of March 31, 2023. In addition to the Company's plans to develop, manufacture and comme rcialize its product candidates, the treatment potential of IMM - 1 - 104, the design, enrollment criteria and conduct of the Phase 1/2a clinical trial, the translation of preclin ical data into human clinical data, the ability of initial clinical data to de - risk IMM - 1 - 104 and be confirmed as the study progresses, including the safety, tolerability, pharmacokinetic s, pharmacodynamics and potential efficacy of IMM - 1 - 104; the potential advantages and effectiveness of the company’s clinical and preclinical candidates, the timing of additiona l trial updates, recommended phase 2 dose and additional safety data, the indications to be pursued by the Company in the Phase 2a portion of the study, the timing of subm iss ion of the IND for IMM - 6 - 415, the filing with, and approval by, regulatory authorities of our product candidates, the sufficiency of funds to operate the business of the Compan y, statements regarding the Company's ability to advance its pipeline and further diversify its portfolio and make progress towards its longstanding goal of creating better m edi cines for cancer patients, the Company’s cash needs and availability, including our revenue streams, projected cash runway and current operating plans, and the plans and o bje ctives of management for future operations. These forward - looking statements are subject to a number of risks, uncertainties and assumptions, including, without limitation: our limited operating history; our history of operating losses; our ability to raise the substantial additional capital that will be required to finance our operations; th e d ifficulty of obtaining regulatory approval for any of our current or future product candidates; our ability to submit an Investigational New Drug application (“IND”), or IND amendment s o r comparable documents in foreign jurisdictions in order to commence clinical trials on the timelines we expect; our limited experience in designing and conducting clinical tri als; the timing of the initiation, progress and potential results of our ongoing and planned preclinical studies and clinical trials and our research programs, including our Ph ase 1/2a clinical trial; our ability to successfully complete our Phase 1/2a clinical trial, or any planned clinical trials and for those trials to produce positive results; the ris k of substantial delays in completing, if at all, the development and commercialization of our current or future product candidates; risks related to adverse events, toxicities or ot her undesirable side effects caused by our current or future product candidates; the risk of delays or difficulties in the enrollment and/or maintenance of patients in clinical tr ials; our substantial reliance on the successful development of our current and future product candidates, as well as our platform, including our proprietary technologies suc h a s DCT and Fluency; risks related to competition in our industry; the market opportunity for our product candidates, if approved; risks related to manufacturing; risks relate d t o our reliance on third parties; risks related to our intellectual property; and risks related to the pandemic related to COVID - 19, its variants and future pandemics. These and other important factors discussed under the caption “Risk Factors” in the Company’s Annual Report on Form 10 - K for the year ended December 31, 2022 filed with the SEC and its other reports filed with the SEC could cause actual results to differ materially from those indicated by the forw ard - looking statements made in this presentation. Any such forward - looking statements represent management’s estimates as of the date of this presentation. While the Company may elec t to update such forward - looking statements at some point in the future, it disclaims any obligation to do so, even if subsequent events cause its views to ch ang e. These forward - looking statements should not be relied upon as representing the Company’s views as of any date subsequent to the date of this presentation. This presentation also contains estimates and other statistical data made by independent parties and by us relating to market si ze and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such data and estimates. In addition, projections, assumptions and estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a h igh degree of uncertainty and risk. Neither we nor our affiliates, advisors or representatives makes any representation as to the accuracy or completeness of that data or u nde rtake to update such data after the date of this presentation. Data of trametinib, cobimetinib , binimetinib , selumetinib , encorafenib and AMG - 510 (now known as sotorasib ) as compared to IMM - 1 - 104 presented in this presentation is based on head - to - head studies where these therapies have been purchased from commercial sources rather than the pharmaceutical company commercializing or developing, as applicable, the compound. FORWARD - LOOKING STATEMENTS AND OTHER DISCLAIMERS

 

Differentiated Approach • Targeting Universal - RAS patient population versus limited single mutation targeted approaches • Once - Daily Oral Dosing • Deep cyclic inhibition targeted, based on: • Manyfold higher C MAX • and short half - life • Approach designed to spare healthy cells and potential to limit adaptive resistance • Monotherapy - Focused initially, with combination potential 3 IMM - 1 - 104 Demonstrated Universal - RAS Potential Key Inflection Points Expected in Near Term • Initial Phase 1 PK, PD, safety data support profile for IMM - 1 - 104 believed to be necessary for Deep Cyclic Inhibition • Investigator enthusiasm high ; broad inclusion criteria • Additional trial updates expected on a periodic basis; RP2D expected in early 2024 • IMM - 6 - 415 IND expected in Q4 2023 • Cash runway projected into Q4 2024 • Robust preclinical activity observed in: • Pancreatic Cancer (KRAS G12C & G12V) • NSCLC (KRAS G12S) • CRC (KRAS G12D) • Melanoma (NRAS Q61R) • And others • Hypothesis for IMM - 1 - 104 from proprietary model that identified counterintuitive and novel deep cyclic inhibition approach • Validated using proprietary bioinformatics & 3D tumor growth assays

 

PROGRAM INDICATION DISCOVERY IND - ENABLING PHASE 1 PHASE 2 PHASE 3 ANTICIPATED MILESTONES IMM - 1 - 104 Universal - RAS Phase 1/2a Trial Enrolling; RP2D expected in early 2024 IMM - 6 - 415 Universal - MAPK IND filing expected in Q4 2023 Multiple additional programs in discovery phase Development Pipeline 4 Once Daily (QD) Twice Daily (BID) Wholly Owned Product Portfolio Differentiated by Indication and Half - life Preliminary estimated Cash, cash equivalents and marketable securities as of March 31, 2023 of $91.5M* projected to fund operations into Q4 2024 *Our actual consolidated financial results as of March 31, 2023 are not yet available. Our financial closing procedures for t he first quarter ended March 31, 2023 are not yet complete and, as a result, our final results upon completion of those procedures may differ materially from our preliminary estimates. The preliminary consolidated financial data presented above as of March 31, 2023 is not a comprehensive statement of our financia l p osition or operating results; reflects our preliminary estimates based on information available as of the date of this presentation; and is subject to chan ge, and those changes may be material. Accordingly, you should not place undue reliance upon these preliminary estimates.

 

IMM - 1 - 104

 

6 IMM - 1 - 104 Target Profile Potential for Universal - RAS Activity Deep Cyclic Inhibition ; Once - Daily Oral Dosing Short plasma half - life to minimize drug trough Initially being developed as Monotherapy Designed to Resist CRAF - bypass in RAS mutant tumors • Phase 1 recruiting all - comer RAS solid tumors: NCT05585320 • First patient dosed November 2022 • Initial Phase 1 PK, PD and safety d ata reported at AACR 2023

 

7 IMM - 1 - 104’s Potential: Universal - RAS * ' * $ * 5 * 6 4 * .5$62WKHU $OOQGLFDWLRQV *(1( 15$6 +5$6 .5$6 NRAS (14.12%) Targeted KRAS G12C • Based on 27,461 out of 148,268 (18.5%) patients with RAS - mutated tumors in the AACR GENIE database, v13.0 • Percentage of overall mutation shown under RAS paralogue. Select mutation percentages within KRAS are shown HRAS (2.78%) KRAS (83.10%) Compared to single - mutation targeted approaches, our Universal - RAS approach potentially addresses a much larger patient population

 

8 MoA Target Engagement GOAL : Prevent MAPK - pathway bypass events, for expanded activity into RAS mutant setting Near - Zero Drug Trough GOAL : Short plasma half - life to improve tolerability and limit adaptive resistance, so every day is a drug holiday Dramatic PK C MAX Pulse GOAL : Achieve many fold higher drug free fraction C MAX to break tumor addiction Deep, Cyclic Inhibition Plasma PK – 5 Day Comparison Days Conceptual illustration of deep cyclic inhibition (purple) vs. chronic pathway ablation (brown)

 

9 Initial Phase 1 PK, PD and Safety Data for IMM - 1 - 104 Short Half - life Observed Observed IMM - 1 - 104 half - life of approximately 2 hours, as projected in Immuneering’s preclinical modeling Deep Cyclic Inhibition (DCI) Initial pharmacokinetic (PK), pharmacodynamic (PD) and safety data support profile for IMM - 1 - 104 believed to be necessary for Deep Cyclic Inhibition (DCI) Significant PK C MAX Significant levels of PK C MAX observed (~1uM free fraction C MAX at 160 mg QD p.o. doses) Safety Data IMM - 1 - 104 well tolerated with no dose - limiting toxicities (DLTs) or serious adverse events (SAEs) observed RP2D Recommended Phase 2 Dose (RP2D) now expected in early 2024 Trial Timeline Acceleration Potentially therapeutic doses of IMM - 1 - 104 now likely to be reached earlier than previously planned due to acceleration of trial timeline Clinical data timeline reported through April 10th, 2023 (i.e., ~20 weeks since first patient dosed) First demonstration of novel deep cyclic inhibition mechanism in humans

 

10 Patient Status Summary for IMM - 1 - 104 Phase 1 Dose Escalation Clinical data timeline reported through April 10th, 2023 (i.e., ~20 weeks since first patient dosed) # Patient RAS Mutation Dose Level Dose C1D1 (t 1/2 ) C1D15 (t 1/2 ) Mean (t 1/2 ) IMM - 1 - 104 Status 1. PANCREATIC KRAS - G12D I 40 mg QD p.o. 1.82 hours 2.10 hours 1.96 hours Off Treatment 2. COLORECTAL KRAS - G12V II 80 mg QD p.o. 1.41 hours 1.43 hours 1.42 hours Off Treatment 3. COLORECTAL NRAS - Q61L III 160 mg QD p.o. 2.04 hours 1.83 hours 1.94 hours Off Treatment 4. COLORECTAL NRAS - Q61K III 160 mg QD p.o. 1.91 hours 1.97 hours 1.94 hours On Treatment 5. PANCREATIC KRAS - G12D IV 320 mg QD p.o. t.b.d. t.b.d. t.b.d. On Treatment • No DLTs or SAEs observed; No drug - related AEs beyond grade 1 have been reported in dose levels III or IV • Early PK data were approximately dose linear with no drug accumulation​ • Actively enrolling patients at 320 mg QD p.o. with 2 additional patients already consented (KRAS - G12V Pancreatic and KRAS - G12S Colorectal)

 

0 3 6 9 12 15 18 21 24 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 0 10 20 30 40 50 60 70 80 90 100 Time (hours) I M M - 1 - 1 0 4 [ n g / m L ] AACR poster PK/PD: Pt.3 & Pt.4 ERK % Baseline Pt.3 PK (ng/mL) p h o s p h o : t o t a l - E R K ( % B a s e l i n e ) Pt.4 PK (ng/mL) Pt.3 p/t-ERK (% baseline) Pt.4 p/t-ERK (% baseline) 87 - 92% ↓ p/t - ERK C max ≳ 2,000 ng/mL C min ≳ 6 - 8 hours 11 ~ 90% Pharmacodynamic Inhibition of pERK • Dose Level III: Cycle 1 Day 1 (C1D1) PK (solid), BK (dotted), and PD (dotted) for patient 3 ( purple ) and 4 ( blue ), both at 160 mg QD p.o. • PK plasma: pre - dose (0), 0.5, 1, 1.5, 2*, 4, 6, 8, 24 hours; PD plasma: PK - matched without 0.5 or 1.5 hours (*poor sample qualit y for Pt.4 at 2 hour) • PD method: A549 (KRAS G12S ) cells were exposed to patient plasma for 2 - hours before quantifying phosphorylated and total ERK and MEK 0 3 6 9 12 15 18 21 24 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 0 10 20 30 40 50 60 70 80 90 100 Time (hours) I M M - 1 - 1 0 4 [ n g / m L ] AACR poster PK/PD: Pt.3 & Pt.4 MEK % Baseline Pt.3 PK (ng/mL) p h o s p h o : t o t a l - M E K ( % B a s e l i n e ) Pt.4 PK (ng/mL) Pt.3 p/t-MEK (% baseline) Pt.4 p/t-MEK (% baseline) IMM - 1 - 104 PK/PD (pMEK) data shows suppression of pathway bypass 55 - 59% ↓ p/t - MEK C max ≳ 2,000 ng/mL C min ≳ 6 - 8 hours ≥ 90% MEK occupancy PK: C max ≳ 1 μM FF PK: C min ≳ 6 - 8 hours Modeled PK/BK, Drug Free - Fraction (FF) † shows high Cmax † Hoare, Sam RJ. "Analyzing kinetic binding data." Assay Guidance Manual [Internet] (2021) IMM - 1 - 104 PK/PD (pERK) shows MAPK pathway suppression

 

IMM - 1 - 104: Phase 1/2 Clinical Trial Plan * Solid tumor, all comer with evidence of RAS mutation ** Simon 2 - Stage Design. Proposed tumor types may change based upon preclinical PGx studies and clinical function review First Time in Humans • RAS mutated Pancreatic (PAAD) (~ 40 pts) • RAS Mutated NSCLC - Adeno (~40 pts) • RAS Mutated, APC wt CRC (~40 pts) • RAS Mutated Melanoma (~40 pts) • RP2D = Recommended Phase 2 Dose • PGx = Pharmacogenomics IND cleared; First patient dosed on Nov 21, 2022 Expansion 2: Expansion 1: Expansion 3 & 4: biomarker stratification Dose Expansion - Phase 2 a ** Dose Escalation Phase 1a * 12 IMM - 1 - 104 (Dual MEK inhibitor) Bayesian Design (mTPI - 2) e scalation in select solid tumor types* Dose Evaluation and RP2D Dose Evaluation Phase 1b* ≤12 patients expected ~12 - 20 patients expected ; “bake off” between dose levels per Project Optimus

 

13 Phase 1 Sites ClinicalTrials.gov Identifier: NCT05585320 MD Anderson Cancer Center › Houston, Texas, United States, 77030 › Principal Investigator: Shubham Pant, MD United States, Texas NEXT Oncology › San Antonio, Texas, United States. 78229 › Principal Investigator: David Sommerhalder , MD MD Weill Cornell Medicine › New York, New York, United States, 10021 › Principal Investigator: Anna Pavlick, DO United States, New York City of Hope › Duarte, California, United States, 91010 › Principal Investigator: Vincent Chung, MD United States, California NEXT Oncology › Fairfax, Virginia, United States, 22031 › Principal Investigator: Alex Spira , MD, PhD United States, Virginia • Investigator enthusiasm remains high • Broad RAS inclusion criteria (Solid Tumors, All Histologies )

 

IMM - 1 - 104 Preclinical Data

 

IMM - 1 - 104 Demonstrated Universal - RAS Potential 15 Humanized 3D - TGA RAS, RAF mutation Response # Non - Response # NRAS G12 2 0 NRAS G13 1 0 NRAS Q61 17 2 KRAS A146 1 0 KRAS G12 36 8 KRAS G13 ^ 3 1 KRAS Q61 3 0 HRAS G13 * 1 0 BRAF (Class I or II) 21 4 Total 85 (85.0%) 15 (15.0%) ^ 1 model also bearing KRAS Q61 /// * 1 model also bearing NRAS Q61 RAS, RAF mutation Response # Non - Response # Not Present 17 15 Total 17 (53.1%) 15 (46.9%) Response to IMM - 1 - 104 based on 3D - TGA and other preclinical modeling. Parallel translational efforts are focused on projecting p atient - aligned molecular profiles or ‘Targetability’. # Models tested in 3D - TGA were assigned responsive if dose response IC50 < 1uM (sensitive) or IC50 ≥ 1 with >25% reduction at 10uM (intermediate), and non - responsive otherwise (resistant) † Select 3D - TGA models: (1.) Pancreatic MIA PaCa - 2 (sensitive/responsive), (2.) Pancreatic Capan - 2 (intermediate/responsive), (3.) Melanoma SK - MEL - 2 (sensitive/responsive), (4.) Lung A549 (intermediate/responsive) Tissue Response # Non - Response # Pancreatic † 17 2 Melanoma † 22 0 Lung † 19 6 CRC 20 5 Thyroid 6 1 Soft Tissue 2 1 Breast 2 6 Gastric 4 2 Ovary 3 2 Prostate 1 2 Fibrosarcoma 1 0 Liver 4 2 Neuroblastoma 1 1 Total 102 (77.3%) 30 (22.7%) Kolitz, et al. 2023 AACR: Targeting RAS Philadelphia, PA 132 Tumor Models 75 = RAS Mutant

 

Humanized 3D - TGA Pharmacogenomics (PGx) Modeling 16 Nair, et al. 2023, AACR: National Meeting, Orlando, FL • Cell lines tested in 3D - TGA (N=132) were assigned response of sensitive (IC50 < 1uM), intermediate (IC50 ≥ 1 and >25% reduction at 10uM), and resistant otherwise • The dark line on each plot represents the median of the individual curves • Vertical gray boxes match C max IMM - 1 - 104 drug free - fractions attained in patients 3 and at 160 mg QD p.o. (both at Dose Level 3 in Phase 1 trial) 0 25 50 75 100 1 10 100 1000 10000 Dose (nM) % E d U ( N o r m a l i z e d t o V e h i c l e C o n t r o l ) 3D TGA Results − Gold Standard IMM−1−104 0 25 50 75 100 1 10 100 1000 10000 Dose (nM) % E d U ( N o r m a l i z e d t o V e h i c l e C o n t r o l ) 3D TGA Results − Gold Standard IMM−1−104 N = 38 Models N = 64 Models N = 30 Models Sensitive Intermediate Resistant Attained Clinical Free Fraction C max of ~1 uM Aligns with 3D - TGA Response Categorization

 

IMM - 1 - 104 Demonstrated Universal - RAS Potential ELN: PJK03-0013PK 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 2750 3000 3250 3500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po IMM-1-104 (TGI = 76%) (TGI = 90%) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Copy of __Pres Data: TV (mm3) - Dose Range - IMM-01-00104 MEDIAN: 0 mg/kg Vehicle QD po : 0 mg/kg Vehicle BID po MEDIAN: 0 mg/kg Vehicle QD po : 100 mg/kg IMM-1-104 BID po MEDIAN: 0 mg/kg Vehicle QD po : 150 mg/kg IMM-1-104 BID po MIA PaCa - 2 N=12 TGI Day21 = 122% TGI Day21 = 108% KRAS G12C PANC 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po A - 549 N=12 TGI Day28 = 95% TGI Day28 = 91% KRAS G12S NSCLC Colon - 26 N=8 TGI Day10 = 108% TGI Day10 = 84% KRAS G12D CRC SK - MEL - 2 N=12 0 3 6 9 12 15 18 21 0 100 200 300 400 500 600 700 800 900 1000 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Mic Drop Panel: TV (mm3) - DR IMM-1-104 MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg IMM-1-104 BID po MEDIAN: 125 mg/kg IMM-1-104 BID po MEDIAN: 150 mg/kg IMM-1-104 BID po TGI Day21 = 100% TGI Day21 = 75% TGI Day21 = 91% NRAS Q61R MEL CRC = colorectal cancer; NSCLC = non - small cell lung cancer; MEL = melanoma; PANC = pancreatic cancer Maximum Effective Dose Range in Mice (plasma t 1/2 = 1.3 hours) is 100 mg/kg to 150 mg/kg BID po Tumor Growth Inhibition (TGI) % = [1 – (Ti – T0)/(Ci – C0)]x100 ; T = treatment groups ; C = control groups *Well - tolerated at top doses with no more than 3 - 6% median body weight loss (BWL) ** Capan - 2 PANC model, as reported at ASCO 2022 (0% TGI for sotorasib and adagrasib at top doses) Well Tolerated : Median Body Weight Loss ≤ 3 - 6%* of baseline at top doses 17 ELN: PJK03-0013PK 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 2750 3000 3250 3500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po IMM-1-104 (TGI = 76%) (TGI = 90%) N=12 KRAS G12V PANC 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Copy of BID Data: TV (mm3) - IMM-1-104 MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg IMM-1-104 BID po MEDIAN: 150 mg/kg IMM-1-104 BID po CAPAN-2 (KRAS-G12V) Capan - 2 TGI Day21 = 84 % TGI Day21 = 61 % IMM - 1 - 104 demonstrated significant and consistent Tumor Growth Inhibition (TGI)

 

Pancreatic: Head - to - Head Comparison of IMM - 1 - 104 +/ - Sotorasib in a KRAS - G12C Pancreatic Tumor Model MIA PaCa - 2 (KRAS G12C ) Pancreatic Xenograft Tumor Model in Athymic Nude Mice Sotorasib was commercially purchased Tumor Growth Inhibition (TGI) % = [1 – (T i – T 0 )/(C i – C 0 )]x100%; Expanded TGI formula vs. previous 1 - [T/C]x100% method IMM - 1 - 104 as compared to sotorasib demonstrated tumor regression, both with insignificant BWL 18 (N=12, per group) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) Copy of __Pres Data: TV (mm3) - 100 - AMG-510 MEDIAN: 0 mg/kg Vehicle QD po : 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg AMG-510 QD po : 0 mg/kg Vehicle BID po Median Body Weight Loss 0% of Baseline 100 mg/kg Shown (N=12, per group) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) Copy of __Pres Data: TV (mm3) - 150 mg - IMM-01-00104 MEDIAN: 0 mg/kg Vehicle QD po : 0 mg/kg Vehicle BID po MEDIAN: 0 mg/kg Vehicle QD po : 150 mg/kg IMM-1-104 BID po 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) Copy of __Pres Data: TV (mm3) - 150 mg - IMM-01-00104 MEDIAN: 0 mg/kg Vehicle QD po : 0 mg/kg Vehicle BID po MEDIAN: 0 mg/kg Vehicle QD po : 150 mg/kg IMM-1-104 BID po (N=12, per group) Median Body Weight Loss < 1.8% of Baseline 150 mg/kg Shown (N=12, per group) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) __Data: TV (mm3) - ALL combinations together 0 mg/kg Vehcile QD po : 0 mg/kg Vehicle BID po 30 mg/kg AMG-510 QD po : 50 mg/kg IMM-1-104 BID po 30 mg/kg AMG-510 QD po : 100 mg/kg IMM-1-104 BID po 30 mg/kg AMG-510 QD po : 150 mg/kg IMM-1-104 BID po IMM - 1 - 104 : Sotorasib 0 : 0 0 : 30 150 : 0 150 : 30 NO TREATMENT + 21 Days 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) __Data: TV (mm3) - ALL combinations together 0 mg/kg Vehicle QD po : 0 mg/kg Vehicle BID po 30 mg/kg sotorasib QD po : 50 mg/kg IMM-1-104 BID po 30 mg/kg sotorasib QD po : 100 mg/kg IMM-1-104 BID po 30 mg/kg sotorasib QD po : 150 mg/kg IMM-1-104 BID po TREATMENT 21 Days Median Body Weight < 1.0% of baseline at top dose combination IMM - 1 - 104 : Sotorasib 50 : 30 100 : 30 150 : 30 Sotorasib 10 - 30 - 100 mg/kg QD p.o.) IMM - 1 - 104 + Sotorasib (50 - 100 - 150 mg/kg BID + 30 mg/kg QD) IMM - 1 - 104 (50 - 100 - 150 mg/kg BID p.o.) IMM - 1 - 104 + Sotorasib (150 mg/kg BID + 30 mg/kg QD) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) __Pres Data: TV (mm3) - 100 - AMG-510 100 mg/kg AMG-510 QD po : 0 mg/kg Vehicle BID po MEDIAN: 0 mg/kg Vehicle QD po : 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg sotorasib QD po : 0 mg/kg Vehicle BID po TGI top - combo = 131% TGI = 122% TGI = 127%

 

Pancreatic: Head - to - Head Comparison of IMM - 1 - 104 vs. Sotorasib and Adagrasib in a KRAS - G12V Pancreatic Tumor Model IMM - 1 - 104 demonstrated tumor regression as compared to no reduction with sotorasib or adagrasib , with insignificant BWL 19 Adagrasib (30, 100 mg/kg QD p.o.) IMM - 1 - 104 (100, 150 mg/kg BID p.o.) Sotorasib (30, 100 mg/kg QD p.o.) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Copy of BID Data: TV (mm3) - IMM-1-104 MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg IMM-1-104 BID po MEDIAN: 150 mg/kg IMM-1-104 BID po CAPAN-2 (KRAS-G12V) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Copy of BID Data: TV (mm3) - IMM-1-104 MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg IMM-1-104 BID po MEDIAN: 150 mg/kg IMM-1-104 BID po CAPAN-2 (KRAS-G12V) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) QD Data: TV (mm3) - AMG-510 Sotorasib MEDIAN: 0 mg/kg Vehicle QD po MEDIAN: 30 mg/kg sotorasib QD po MEDIAN: 100 mg/kg sotorasib QD po CAPAN-2 (KRAS-G12V) (N=12, per group) (N=12, per group) (N=12, per group) 0 3 6 9 12 15 18 21 0 50 100 150 200 250 300 350 400 450 500 550 600 650 700 750 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) QD Data: TV (mm3) - AMG-510 Sotorasib MEDIAN: 0 mg/kg Vehicle QD po MEDIAN: 30 mg/kg sotorasib QD po MEDIAN: 100 mg/kg sotorasib QD po CAPAN-2 (KRAS-G12V) Capan - 2 (KRAS G12V ) Pancreatic Xenograft Tumor Model in Athymic Nude Mice Sotorasib and adagrasib were commercially purchased Tumor Growth Inhibition (TGI) % = [1 – (T i – T 0 )/(C i – C 0 )]x100%; Expanded TGI formula vs. previous 1 - [T/C]x100% method Median Body Weight Loss 0% of Baseline Median Body Weight Loss 0% of Baseline Median Body Weight Loss <5.8% of Baseline

 

Dummer, et al 2017 Lancet S1470 - 2045 (17) 30180 - 8 2.8 months 1.5 months 11.0 months 10.1 months Binimetinib Dacarbazine Hazard Ratio Progression Free Survival Overall Survival 0.62 1.00 NRAS Status Binimetinib Dacarbazine N = 269 N = 133 Q61K 100 (37%) 51 (38%) Q61L 32 (12%) 17 (13%) Q61R 137 (51%) 64 (48%) Wildtype 0 1 (1%) Serious Adverse Events (34% binimetinib vs. 22% dacarbazine) Overall Response Rate (ORR: 15% binimetinib vs. 7% dacarbazine) Melanoma: Phase 3 NEMO Study: Binimetinib vs. Dacarbazine (NRAS mut Melanoma) Summary of Phase 3 NEMO study of Binimetinib as reported in Lancet (c.2017) - a potential opportunity for IMM - 1 - 104 20 2: 1

 

Melanoma: Head - to - Head NRAS - Q61R Melanoma Xenograft Study: Binimetinib vs. IMM - 1 - 104 in SK - MEL - 2 IMM - 1 - 104 as compared to binimetinib monotherapy demonstrated greater tumor growth inhibition (TGI) SK - MEL - 2 (NRAS - Q61R) Melanoma Xenograft Tumor Model in Athymic Nude Mice CRAF - bypass IMM - 1 - 104 (100 - 125 - 150 mg/kg BID p.o.) Binimetinib (3 - 10 - 30 mg/kg BID p.o.) 0 1 2 3 4 5 6 7 8 9 10111213141516171819202122 0 100 200 300 400 500 600 700 800 900 1000 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) SK-MEL-2 (NRAS-mutant MEL) - IMM-1-104 MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg IMM-1-104 BID po MEDIAN: 125 mg/kg IMM-1-104 BID po MEDIAN: 150 mg/kg IMM-1-104 BID po 0 1 2 3 4 5 6 7 8 9 10111213141516171819202122 0 100 200 300 400 500 600 700 800 900 1000 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) SK-MEL-2 (NRAS-mutant MEL) - Binimetinib MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 3 mg/kg Binimetinib BID po MEDIAN: 10 mg/kg Binimetinib BID po MEDIAN: 30 mg/kg Binimetinib BID po 0 1 2 3 4 5 6 7 8 9 10111213141516171819202122 0 100 200 300 400 500 600 700 800 900 1000 Time (days) T u m o r v o l u m e ( M e d i a n ± I n t e r q u a r t i l e ; m m 3 ) SK-MEL-2 (NRAS-mutant MEL) - IMM-1-104 MEDIAN: 0 mg/kg Vehicle BID po MEDIAN: 100 mg/kg IMM-1-104 BID po MEDIAN: 125 mg/kg IMM-1-104 BID po MEDIAN: 150 mg/kg IMM-1-104 BID po N=12, per group N=12, per group TGI = 100% TGI = 91% TGI = 75% TGI = 35% 21 Binimetinib was commercially purchased

 

CRC: Head - to - Head Comparison of IMM - 1 - 104 Against Selumetinib and Binimetinib in a KRAS - G12D CRC Syngeneic Mouse Tumor Model 0 3 6 9 12 15 18 21 24 27 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Data: TV (mm3) - Selumetinib - 50 only Vehicle 0 mg/kg BID po 50 mg/kg BID po Selumetinib 50 mg/kg BID po Selumetinib - Individual 0 3 6 9 12 15 18 21 24 27 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) Data: TV (mm3) - Binimetinib - 30 dose only Vehicle 0 mg/kg BID po 30 mg/kg BID po Binimetinib 30 mg/kg BID po Binimetinib - Individual Colon - 26 (KRAS - G12D) Syngeneic Colorectal Tumor Model in Balb/c Mice Selumetinib and binimetinib were commercially purchased Tumor Growth Inhibition (TGI) % = [1 – (Ti – T0)/(Ci – C0)]x100%; Expanded TGI formula vs. previous 1 - [T/C]x100% method IMM - 1 - 104 demonstrated greater tumor growth inhibition (TGI), lower body weight loss (BWL) and greater durability via reductions in tumor volume (TV) IMM - 1 - 104 (Clinical) Binimetinib (FDA approved) Selumetinib (FDA approved) 22 N=8, per group N=8, per group N=8, per group

 

IMM - 6 - 415

 

IMM - 6 - 415: Monotherapy Activity in RAF and RAS Mutant Tumors Colon - 26 A - 549 SK - MEL - 2 A - 375 KRAS G12S NSCLC KRAS G12D CRC NRAS Q61R MEL BRAF V600E MEL CRC = colorectal cancer; NSCLC = non - small cell lung cancer; MEL = melanoma SITC 2022 Presentation: Maximum Effective Dose Range in Mice ( plasma t 1/2 = 0. 3 to 0.4 hours ): 150 - 180 mg/kg BID Well Tolerated up to Maximum Monotherapy Effective Dose Range of 150 to 180 mg/kg 24 Model HRAS NRAS BRAF NF1 3D-TGA SK-MEL-2 p.Q61R MM127 p.G13R p.G464E n.t. MM415 p.Q61L n.t. MEL-JUSO p.G13D p.Q61L n.t. SK-MEL-30 p.Q61K n.t. Hs852T p.G12V n.t. MeWo LoF n.t. A375 p.V600E SK-MEL-28 p.V600E 3D - Tumor Growth Assay (3D - TGA) sensitivity (green) SK - MEL - 28 BRAF V600E MEL 0 2 4 6 8 10 12 14 16 18 20 22 0 200 400 600 800 1000 1200 1400 1600 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e o r I n d i v i d u a l ; m m 3 ) A549 (KRAS G12S ) 180 mg/kg BID PO MEDIAN: IMM-6-415, 180mg/kg, 10ul/g, p.o., BID × 21 MEDIAN: Vehicle, 0mg/kg, 10ul/g, p.o., BID x 21 IMM-6-415, 180mg/kg, 10ul/g, p.o., BID × 21 N = 12 mice per group ** **** ** P = 0.0015; day 7 **** P < 0.0001; day 10-21 **** **** **** 1104 mm 3 197 mm 3 138 mm 3 2-way ANOVA followed by Tukey for mulitple comparisons

 

Accelerated Cadence of IMM - 6 - 415 Enhanced Activity of Checkpoint Inhibitors Cyclic disruption of MEK improved overall survival with check point inhibitors (SITC 2022) 25 Schedule Dose (mg/kg) Veh ⍺ PD - 1 (BIW) ⍺ CTLA - 4 (BIW) IMM - 6 - 415 IMM - 6 - 415 + PD - 1 IMM - 6 - 415 + CTLA - 4 BID 120 0/12 7/12 11/12 10/12 BID 60 0/12 0/12 8/12 8/12 BID 30 0/12 0/12 5/12 5/12 QD 120 0/12 0/12 7/12 7/12 QD 60 0/12 1/12 4/12 8/12 QD 30 0/12 0/12 6/12 7/12 BIW 10 0/12 4/12 BIW 10 0/12 4/12 • Number of BALB/c mice (out of 12) with tumors through Day 28 with volumes lower than 2,000 mm 3 Monotherapy Treated Alive at Day 28 Combination ≥ 3 Advantage Syngeneic CT - 26 Model KRAS G12D CRC Presented at SITC (Nov. 2022): RAS wild type MC38 IO model ≥3 advantage only observed in IMM - 6 - 415 (120 p.o. BID) + anti - PD - 1

 

Corporate

 

• Preliminary estimated Cash, cash equivalents and marketable securities as of March 31, 2023: $91.5M* • Cash runway projected into Q4 2024 supports: • IMM - 1 - 104: • Multiple data readouts from Phase 1/2a trial • IMM - 6 - 415: • Anticipate IND filing in Q4 2023 • Research in additional oncology programs 27 Finance & Intellectual Property Finance Intellectual Property** Patents issued/pending: • Pending U.S. and ex - U.S. applications relating to IMM - 1 - 104 • Pending U.S. provisional and PCT applications relating to IMM - 6 - 415 • Issued U.S. patent and pending application relating to DCT • Pending U.S. applications to Fluency Expected patent expiration: (excluding patent term adjustments, etc.) • IMM - 1 - 104 = 2041 • IMM - 6 - 415 = 2043 • DCT = 2039 • Fluency = 2039 *Our actual consolidated financial results as of March 31, 2023 are not yet available. Our financial closing procedures for t he first quarter ended March 31, 2023 are not yet complete and, as a result, our final results upon completion of those procedures may differ materially from our preliminary estimates. Th e preliminary consolidated financial data presented above as of March 31, 2023 is not a comprehensive statement of our financial position or operating results; reflects our prel imi nary estimates based on information available as of the date of this presentation; and is subject to change, and those changes may be material. Accordingly, you should not place un due reliance upon these preliminary estimates. **As reported in the Company's most recent Annual Report on Form 10 - K filed with the SEC

 

28 Milestones Program Milestone Expected Timing IMM - 1 - 104 Initial Phase 1 pharmacokinetic (PK) and safety data COMPLETE IMM - 1 - 104 Initial Phase 1 pharmacodynamic (PD) modeling data and additional PK and safety data COMPLETE IMM - 1 - 104 Additional trial updates On a periodic basis IMM - 1 - 104 RP2D and Additional Safety data Early 2024 IMM - 6 - 415 IND filing Q4 2023

 

Differentiated Approach • Targeting Universal - RAS patient population versus limited single mutation targeted approaches • Once - Daily Oral Dosing • Deep cyclic inhibition targeted, based on: • Manyfold higher C MAX • and short half - life • Approach designed to spare healthy cells and potential to limit adaptive resistance • Monotherapy - Focused initially, with combination potential 29 IMM - 1 - 104 Demonstrated Universal - RAS Potential Key Inflection Points Expected in Near Term • Initial Phase 1 PK, PD, safety data support profile for IMM - 1 - 104 believed to be necessary for Deep Cyclic Inhibition • Investigator enthusiasm high ; broad inclusion criteria • Additional trial updates expected on a periodic basis; RP2D expected in early 2024 • IMM - 6 - 415 IND expected in Q4 2023 • Cash runway projected into Q4 2024 • Robust preclinical activity observed in: • Pancreatic Cancer (KRAS G12C & G12V) • NSCLC (KRAS G12S) • CRC (KRAS G12D) • Melanoma (NRAS Q61R) • And others • Hypothesis for IMM - 1 - 104 from proprietary model that identified counterintuitive and novel deep cyclic inhibition approach • Validated using proprietary bioinformatics & 3D tumor growth assays

 

Appendix Nasdaq: IMRX April 2023

 

Our Platform Converts Gene Expression to Counterintuitive Insights Goal: achieve broader activity and better tolerability in RAS and beyond mutant disease Disease Cancellation Disease Amplification Disease Cancellation Disease Amplification 1 st generation MEKi 1 st generation MEKi IMRX Disease Cancelling Technology - US Patent 11,043,305 Unlike first generation MEK inhibitors, IMM - 1 - 104 is designed to prevent RAF - and KSR - mediated activation of MEK (i.e., CRAF - bypass) and displays a short plasma half - life to potentially drive deep cyclic inhibition of the pathway. Data - driven Identification and Optimization of New Medicines to Cancel Cancer Cachexia Presented by Ben Zeskind at the 12 th International Conference of Cachexia, Sarcopenia & Muscle Wasting (SCWD) in Berlin, Dec. 6 - 8, 2019 31 Cancer Cell Growth RAS RAF MEK ERK NF1 OFF ON RAS NANOCLUSTERS P P P P P P P MEK inh RTK

 

Deep Cyclic Inhibition Demonstrated Using Transcriptomics Traditional Approach Signaling Dynamics Chronic Suppression → TOXICITY Cyclic Disruption → TOLERABILITY 32 Syngeneic Colon - 26 study (18 days BID dosing; tumor RNA) Syngeneic Colon - 26 study (18 days BID dosing; tumor RNA)

 

IMM - 1 - 104 is a Dual - MEK Inhibitor Goal deep, cyclic inhibition with ability to prevent MEK - reactivation (improve tolerability and activity) Short plasma half - life to minimize drug trough (~ 1 to 2 hours t 1/2 ) Resists CRAF - bypass in RAS mutant tumors (↓ pERK and pMEK) Ideal Dosing Schedule: ≥ 7 - 8 half lives between doses (BID for < 1.5 hr t 1/2 ; QD for 2 to 3 hr t 1/2 ) IMM - 1 - 104 Mechanism Half - Life + 33 Cadence

 

Head - to - Head Comparison of IMM - 1 - 104 Against FDA - Approved MEK Inhibitors: CRAF - Bypass Resistance FDA - Approved MEK inhibitors: Trametinib, Cobimetinib, Binimetinib, Selumetinib commercially purchased 1.00 0.03 0.19 0.17 0.21 0.29 1.00 1.24 6.46 2.96 2.45 0.56 0.01 0.10 1.00 10.00 0.1% DMSO Trametinib Cobimetinib Binimetinib Selumetinib IMM-1-104 p - P r o t e i n : t o t a l P r o t e i n ( N o r m a l i z e d t o D M S O ) Drug Dose = 100 nM (2 hours exposure; A549) A549 KRAS-mut Lung Cancer: pERK and pMEK pERK pMEK CRAF-bypass if > 1.0 Decreased activity for both MEK & ERK A549 KRAS - mut Lung Cancer: pERK and pMEK CRAF Bypass > 1.0 34 Cancer Cell Growth RAS RAF MEK ERK NF1 OFF ON RAS NANOCLUSTERS P P P P P P P MEK inh RTK

 

Head - to - Head Comparison of IMM - 1 - 104 Against Binimetinib +/ - Encorafenib in KRAS - G12S NSCLC Tumor Model A549 (KRAS G12S ) NSCLC Xenograft Tumor Model in Athymic Nude Mice Tumor Growth Inhibition (TGI) % = [1 – ( T i – T 0 )/(C i – C 0 )]x100%; Expanded TGI formula vs. previous 1 - [T/C]x100% method Human Dose Equivalent (HDE) binimetinib = 1 - 3 mg/kg BID IMM - 1 - 104 as compared to binimetinib monotherapy demonstrated greater tumor growth inhibition (TGI) Binimetinib and encorafenib were commercially purchased IMM - 1 - 104 (150 mg/kg BID p.o.) (N=12, per group) 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po IMM - 1 - 104 (TGI = 95%) IMM - 1 - 104 (TGI = 91%) Binimetinib + Encorafenib (10 mg/kg BID + 60 mg/kg QD p.o.) (N=12, per group) Encorafenib (TGI = 41%) minus 1 TV limit Binimetinib (TGI = 79%) Bin + Enc (TGI = 62%) 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 60 mpk QD:10 mpk BID - E:B MEDIAN Vehicle 0 mg/kg QD po : Vehicle 0 mg/kg BID po MEDIAN 60 mg/kg Encorafenib QD po : Vehicle 0 mg/kg BID po MEDIAN Vehicle 0 mg/kg QD po : 10 mg/kg Binimetinib BID po MEDIAN 60 mg/kg Encorafenib QD po : 10 mg/kg Binimetinib BID po 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 60 mpk QD:10 mpk BID - E:B MEDIAN Vehicle 0 mg/kg QD po : Vehicle 0 mg/kg BID po MEDIAN 60 mg/kg Encorafenib QD po : Vehicle 0 mg/kg BID po MEDIAN Vehicle 0 mg/kg QD po : 10 mg/kg Binimetinib BID po MEDIAN 60 mg/kg Encorafenib QD po : 10 mg/kg Binimetinib BID po 35

 

Head - to - Head Comparison of IMM - 1 - 104 versus Binimetinib +/ - Encorafenib in BRAF - V600E Melanoma Tumor Model A375 (BRAF V600E ) Melanoma Xenograft Tumor Model in Athymic Nude Mice Tumor Growth Inhibition (TGI) % = [1 – ( T i – T 0 )/(C i – C 0 )]x100%; Expanded TGI formula vs. previous 1 - [T/C]x100% method Human Dose Equivalent (HDE) binimetinib 1 - 3 mg/kg BID IMM - 1 - 104 as compared to binimetinib monotherapy demonstrated greater tumor growth inhibition (TGI) Binimetinib and encorafenib were commercially purchased IMM - 1 - 104 (100 & 150 mg/kg BID p.o.) (N=12, per group) Binimetinib + Encorafenib (10 mg/kg BID + 60 mg/kg QD p.o.) (N=12, per group) IMM - 1 - 104 (TGI = 80%) (TGI = 96%) Encorafenib (TGI = 99%) Binimetinib (TGI = 51%) Bin + Enc (TGI = 107%) Tumor Volume (Median ± quartile; mm 3 ) 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 2750 3000 3250 3500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 60 mpk QD:10 mpk BID - E:B MEDIAN Vehicle 0 mg/kg QD po : Vehicle 0 mg/kg BID po MEDIAN 60 mg/kg Encorafenib QD po : Vehicle 0 mg/kg BID po MEDIAN Vehicle 0 mg/kg QD po : 10 mg/kg Binimetinib BID po MEDIAN 60 mg/kg Encorafenib QD po : 10 mg/kg Binimetinib BID po 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 0 250 500 750 1000 1250 1500 1750 2000 2250 2500 2750 3000 3250 3500 Time (days) T u m o r v o l u m e ( M e d i a n ± Q u a r t i l e ; m m 3 ) **Data: TV (mm3) - 100 + 150 mpk - IMM-1-104 MEDIAN Vehicle 0 mg/kg BID po MEDIAN 150 mg/kg IMM-01-00104 BID po MEDIAN 100 mg/kg IMM-01-00104 BID po Tumor Volume (Median ± quartile; mm 3 ) 36

 

Conclusions (NRAS mutant Melanoma) In the phase 3 NEMO study published in Lancet (c. 2017), binimetinib failed to substantially improve overall survival vs. dacarbazine (11.0 vs. 10.1 months) in NRAS mutant melanoma patients and led to a ~50% increase in serious adverse events (34% vs. 22%). The most common NRAS mutation in the NEMO study was Q61R. We further compared binimetinib vs. IMM - 1 - 104 in vivo using SK - MEL - 2 (NRAS - Q61R). Collectively, our data suggest that binimetinib may not effectively control MAPK pathway reactivation in RAS mutant tumors. In contrast, the deep cyclic inhibition combined with a dual - MEK mechanism of action of IMM - 1 - 104 may offer a unique therapeutic advantage over first generation MEK inhibitors in RAS mutant tumors. 37

 

38 RAS Mutation Profiles Within Select Tumor Indications • Based on given tumor type of patients with RAS - mutated tumors in the AACR GENIE database, v13.0 • Each RAS paralogue shown as percent overall RAS mutant tumors within each indication • Presented at 2023 AACR: Targeting RAS. Kolitz, et al. (Philadelphia, PA) 4 5 4 . 4 / 4 + * 5 * ' * ' 15$6RWKHU 4 . +5$6RWKHU * & * ' * $ * 5 * 6 * 9 4 * .5$62WKHU 0HODQRPD *(1( 15$6 +5$6 .5$6 * & * $ * 6 4 * .5$62WKHU 3DQFUHDWLF$GHQRFDUFLQRPD *(1( 15$6 +5$6 .5$6 * $ * 5 * 6 4 * .5$62WKHU /XQJ$GHQRFDUFLQRPD *(1( 15$6 +5$6 .5$6 Pancreatic Cancer NRAS = 0.34% HRAS = 0.06% KRAS = 99.60% NRAS = 2.67% HRAS = 0.31% KRAS = 97.02% Lung Cancer Melanoma Colorectal Cancer NRAS = 89.14% HRAS = 5.29% KRAS = 5.57% NRAS = 8.25% HRAS = 0.24% KRAS = 91.51% 4 . * ' 4 5 15$6RWKHU * & * $ * 5 * 6 4 * .5$62WKHU &RORUHFWDO$GHQRFDUFLQRPD *(1( 15$6 +5$6 .5$6

 

KRAS Mutant Pancreatic (PAAD): Translational Opportunity GENIE cohort v13.0 - public The AACR Project GENIE Consortium. AACR Project GENIE: Powering Precision Medicine Through An International Consortium, Cance r D iscov. 2017 Aug;7(8):818 - 831 ↑ Resistance Mixed Sensitive Have Altered KRAS: Biomarker Positive Biomarker Sensitive Profile (80.2% overall) Biomarker Resistant Profile (0.6% overall) † Further Biomarker Stratification Not Required † PANCREATIC Patients Patient mapping with 3D - TGA Translational Step : Assess sensitivity of a panel of cell lines in the 3D - TGA; determine key mutations present in each Bioinformatics Step : How many patients does each cell line represent, based on key mutations present in each 39

 

NRAS Mutant Melanoma: Translational Opportunity ↑ Resistance Mixed Sensitive Have Altered NRAS: Biomarker Positive Biomarker Sensitive Profile (19% overall) Biomarker Resistant Profile (0.8% overall) † Further Biomarker Stratification Not Required † MELANOMA Patients GENIE cohort v13.0 - public The AACR Project GENIE Consortium. AACR Project GENIE: Powering Precision Medicine Through An International Consortium, Cance r D iscov. 2017 Aug;7(8):818 - 831 Patient mapping with 3D - TGA Translational Step : Assess sensitivity of a panel of cell lines in the 3D - TGA; determine key mutations present in each Bioinformatics Step : How many patients does each cell line represent, based on key mutations present in each 40

 

KRAS Mutant NSCLC (Adeno): Translational Opportunity Have Altered KRAS: Biomarker Positive Biomarker Sensitive Profile (21.5% overall) Biomarker Resistant Profile (Refine Subsets) NSCLC - Ad Patients † ↑ Resistance (Further Refine Subsets) Sensitive † Consider Further Biomarker Stratification GENIE cohort v13.0 - public The AACR Project GENIE Consortium. AACR Project GENIE: Powering Precision Medicine Through An International Consortium, Cance r D iscov. 2017 Aug;7(8):818 - 831 Patient mapping with 3D - TGA Translational Step : Assess sensitivity of a panel of cell lines in the 3D - TGA; determine key mutations present in each Bioinformatics Step : How many patients does each cell line represent, based on key mutations present in each 41

 

KRAS Mutant CRC: Translational Opportunity Have Altered KRAS: Biomarker Positive Biomarker Sensitive Profile (9.3% overall) Biomarker Resistant Profile (Refine Subsets) CRC Patients † ↑ Resistance (Further Refine Subsets) Sensitive † Further Refine Biomarker Stratification GENIE cohort v13.0 - public The AACR Project GENIE Consortium. AACR Project GENIE: Powering Precision Medicine Through An International Consortium, Cance r D iscov. 2017 Aug;7(8):818 - 831 Patient mapping with 3D - TGA Translational Step : Assess sensitivity of a panel of cell lines in the 3D - TGA; determine key mutations present in each Bioinformatics Step : How many patients does each cell line represent, based on key mutations present in each 42

 

Translating IMM - 1 - 104’s Universal - RAS Potential (AACR GENIE ® ) 43 Nair, et al. 2023, AACR: National Meeting, Orlando, FL MAPK + = GENIE patients per indication with activation mutation in KRAS, NRAS, HRAS, BRAF (class I or II), based on 3D - TGA PGx Modeling 0$3.0XWDWHG 1 0$3.:7 1 3$$' 1XPEHURI*(1( 3DWLHQWV RI*(1( 3DWLHQWV PANCREATIC Lower Response Potential | Higher Response Potential Biomarker vs. Population Mutations PAAD For 122 3 D - TGA cell lines where in - house WES data were also collected, the upper plateau - to - 1 uM difference was used to delineate responder from non - responder, and thus train a logistic regression model with 10 - fold cross validation . There were 28 features used, one comprised of a consolidated MAPK mutations status (mutations in K/H/NRAS, GNAQ/ 11 , and BRAF class I/II), and 27 other genes representing key pathways . With an AUC of 0 . 84 on the training cohort and 0 . 72 on test cohort, the model was then applied to GENIE cohorts (above) where all features were included on the testing panel . For each indication of interest, a kernel density plot of the probability of predicted response for the entire cohort (projected onto the negative y - axis), and the MAPK(+) subset (positive y - axis) shows enrichment for higher probability of response with restriction to MAPK alteration status .

 

Translating IMM - 1 - 104’s Universal - RAS Potential (AACR GENIE ® ) 44 Nair, et al. 2023, AACR: National Meeting, Orlando, FL MAPK + = GENIE patients per indication with activation mutation in KRAS, NRAS, HRAS, BRAF (class I or II), based on 3D - TGA PGx Modeling For 122 3 D - TGA cell lines where in - house WES data were also collected, the upper plateau - to - 1 uM difference was used to delineate responder from non - responder, and thus train a logistic regression model with 10 - fold cross validation . There were 28 features used, one comprised of a consolidated MAPK mutations status (mutations in K/H/NRAS, GNAQ/ 11 , and BRAF class I/II), and 27 other genes representing key pathways . With an AUC of 0 . 84 on the training cohort and 0 . 72 on test cohort, the model was then applied to GENIE cohorts (above) where all features were included on the testing panel . For each indication of interest, a kernel density plot of the probability of predicted response for the entire cohort (projected onto the negative y - axis), and the MAPK(+) subset (positive y - axis) shows enrichment for higher probability of response with restriction to MAPK alteration status . 0$3.0XWDWHG 1 0$3.:7 1 6.&00(/ 1XPEHURI*(1( 3DWLHQWV RI*(1( 3DWLHQWV MELANOMA Lower Response Potential | Higher Response Potential Biomarker vs. Population Mutations SKCM MEL

 

Translating IMM - 1 - 104’s Universal - RAS Potential (AACR GENIE ® ) 45 Nair, et al. 2023, AACR: National Meeting, Orlando, FL MAPK + = GENIE patients per indication with activation mutation in KRAS, NRAS, HRAS, BRAF (class I or II), based on 3D - TGA PGx Modeling For 122 3 D - TGA cell lines where in - house WES data were also collected, the upper plateau - to - 1 uM difference was used to delineate responder from non - responder, and thus train a logistic regression model with 10 - fold cross validation . There were 28 features used, one comprised of a consolidated MAPK mutations status (mutations in K/H/NRAS, GNAQ/ 11 , and BRAF class I/II), and 27 other genes representing key pathways . With an AUC of 0 . 84 on the training cohort and 0 . 72 on test cohort, the model was then applied to GENIE cohorts (above) where all features were included on the testing panel . For each indication of interest, a kernel density plot of the probability of predicted response for the entire cohort (projected onto the negative y - axis), and the MAPK(+) subset (positive y - axis) shows enrichment for higher probability of response with restriction to MAPK alteration status . ȫ ȫ ȫ 00 3DWLHQW3URMHFWLRQIRU5HVSRQVHLQ*(1(&RKRUWV /8$' 0$3.0XWDWHG 1 0$3.:7 1 /8$' 1XPEHURI*(1( 3DWLHQWV RI*(1( 3DWLHQWV LUNG Lower Response Potential | Higher Response Potential All Patients | Biomarker + Biomarker vs. Population Mutations LUAD

 

Translating IMM - 1 - 104’s Universal - RAS Potential (AACR GENIE ® ) 46 Nair, et al. 2023, AACR: National Meeting, Orlando, FL MAPK + = GENIE patients per indication with activation mutation in KRAS, NRAS, HRAS, BRAF (class I or II), based on 3D - TGA PGx Modeling For 122 3 D - TGA cell lines where in - house WES data were also collected, the upper plateau - to - 1 uM difference was used to delineate responder from non - responder, and thus train a logistic regression model with 10 - fold cross validation . There were 28 features used, one comprised of a consolidated MAPK mutations status (mutations in K/H/NRAS, GNAQ/ 11 , and BRAF class I/II), and 27 other genes representing key pathways . With an AUC of 0 . 84 on the training cohort and 0 . 72 on test cohort, the model was then applied to GENIE cohorts (above) where all features were included on the testing panel . For each indication of interest, a kernel density plot of the probability of predicted response for the entire cohort (projected onto the negative y - axis), and the MAPK(+) subset (positive y - axis) shows enrichment for higher probability of response with restriction to MAPK alteration status . ȫ ȫ 00 3DWLHQW3URMHFWLRQIRU5HVSRQVHLQ*(1(&RKRUWV &2$'5($'&2$'5($' 0$3.0XWDWHG 1 0$3.:7 1 &2$'5($'&2$'5($' 1XPEHURI*(1( 3DWLHQWV RI*(1( 3DWLHQWV COLORECTAL Lower Response Potential | Higher Response Potential Biomarker vs. Population Mutations COAD READ COADREAD All Patients | Biomarker +

 

Translating IMM - 1 - 104’s Universal - RAS Potential (AACR GENIE ® ) 47 Nair, et al. 2023, AACR: National Meeting, Orlando, FL MAPK + = GENIE patients per indication with activation mutation in KRAS, NRAS, HRAS, BRAF (class I or II), based on 3D - TGA PGx Modeling For 122 3 D - TGA cell lines where in - house WES data were also collected, the upper plateau - to - 1 uM difference was used to delineate responder from non - responder, and thus train a logistic regression model with 10 - fold cross validation . There were 28 features used, one comprised of a consolidated MAPK mutations status (mutations in K/H/NRAS, GNAQ/ 11 , and BRAF class I/II), and 27 other genes representing key pathways . With an AUC of 0 . 84 on the training cohort and 0 . 72 on test cohort, the model was then applied to GENIE cohorts (above) where all features were included on the testing panel . For each indication of interest, a kernel density plot of the probability of predicted response for the entire cohort (projected onto the negative y - axis), and the MAPK(+) subset (positive y - axis) shows enrichment for higher probability of response with restriction to MAPK alteration status .