Exhibit 99.2

1 Black Diamond Therapeutics, Inc. Developing MasterKey Therapies to Defeat Cancer Resistance March 19, 2025

2 Forward - Looking Statements This presentation contains forward looking statements of Black Diamond Therapeutics, Inc (“we,” “us,” “our”) within the meaning of the Private Securities Litigation Reform Act of 1995 . Forward looking statements include all statements that are not historical facts, and in some cases, can be identified by terms such as “may,” “might,” “will,” “could,” “would,” “should,” “expect,” “intend,” “plan,” “objective,” “anticipate,” “believe,” “estimate,” “predict,” “potential,” “continue,” “ongoing,” or the negative of these terms, or other comparable terminology intended to identify statements about the future . Forward looking statements contained in this presentation include, but are not limited to, statements regarding our future financial or business performance, conditions, plans, prospects, trends or strategies and other financial and business matters, the continued development and advancement of BDTX - 1535 , the progress, timing and success of our clinical trials of BDTX - 1535 and any of our future product candidates, including the availability, timing and announcement of data and results of such trials, our ability to replicate results achieved in our preclinical studies or clinical trials, the expected timing for regulatory feedback and the disclosure of potential registrational pathways for BDTX - 1535 , the potential of BDTX - 1535 to address the unmet medical need for newly diagnosed non - small cell lung cancer (“NSCLC”) patients with non - classical EGFR mutations and benefit patients with NSCLC across multiple lines of therapy, the potential future development plans for BDTX - 1535 in NSCLC and glioblastoma, the competitive landscape and market for BDTX - 1535 or any of our other current or future product candidates, our ability to maintain our intellectual property portfolio, and the timing and success of our development and commercialization of our product candidates, including our ability to establish and maintain collaborations or strategic relationships . New risks and uncertainties may emerge from time to time, and it is not possible to predict all risks and uncertainties . Except as required by law, we assume no obligation to update these forward looking statements publicly, or to update the reasons actual results could differ materially from those anticipated in the forward looking statements, even if new information becomes available in the future . For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward looking statements, see the section entitled “Risk Factors” in our most recent annual report on Form 10 - K filed with the Securities and Exchange Commission (the “SEC”), as well as discussions of potential risks, uncertainties, and other important factors in our other subsequent filings with the SEC . In addition, we have not conducted any head to head studies comparing our product candidates to any third party drug products or candidates, whether investigated or approved . Information regarding other drug products in this presentation is meant to provide context for illustrative purposes only . Because there are no head to head studies, no conclusions should be made based on cross study comparisons . Recipients are cautioned not to place undue reliance on these forward looking statements, which speak only as of the date such statements are made and should not be construed as statements of fact . This presentation also contains information using industry publications that generally state that the information contained therein has been obtained from sources believed to be reliable, but such information may not be accurate or complete . While we are not aware of any misstatements regarding the information from these industry publications, we have not independently verified any of the data from third party sources nor have we ascertained the underlying economic assumptions relied on therein .

3 Cancer is a Complex and Ever - Evolving Disease Current targeted therapies were designed against a limited subset of oncogenic mutations Increasing adoption of liquid biopsies reveals a broader set of oncogenic mutations We are Developing MasterKey Therapies to Defeat Cancer Resistance MasterKey approach aims to provide one solution for many mutations and expand addressable patient population Our oral therapies are designed so that patients have the opportunity for a longer, healthier, active life

4 Black Diamond Therapeutics At - a - Glance Clinical - stage company advancing MasterKey therapies designed to expand the addressable patient population Experienced team with deep understanding of cancer biology and oncology drug development BDTX - 1535: best/first - in - class 4 th - generation EGFRi for NSCLC , with additional opportunity in GBM Multiple clinical catalysts including BDTX - 1535 Phase 2 data in 1L NSCLC patients in Q4 2025 Pipeline of oral, brain penetrant drug candidates selectively targeting families of oncogenic mutations Lean organization with runway into Q4 2027; ended 2024 with $98.6M, + $70M from BDTX - 4933/Servier deal

5 MasterKey: One Solution for Many Mutations Expanded addressable patient population Black Diamond Approach: Targeting families of oncogenic mutations Limited addressable patient population 5 Brain - penetrant to treat CNS disease Traditional Approach: Targeting single mutations in individual tumor types Potent against broad mutation families (including drug resistance mutations) Selective targeting to deliver well - tolerated therapies

6 Advancing Pipeline Across Multiple Oncology Indications Target Drug Candidate Indication Pre - clinical Phase 1 Phase 2 Phase 3 EGFR RAF BDTX - 1535 BDTX - 4933 2L/3L NSCLC 1L NSCLC FGFR2/3 BDTX - 4876 Achondroplasia or solid tumors RAF/RAS mutant solid tumors Final Phase 2 data expected H1 2026 Phase 0/1 data in recurrent GBM @ AACR April 2025 Partnering opportunity Out - licensed to Servier Q1 2025 GBM Initial Phase 2 data expected Q4 2025

7 Targets a broad spectrum of EGFR classical, non - classical, and C797S resistance mutations BDTX - 1535 MasterKey BDTX - 1535: Potential First and Best - in - Class 4th Generation EGFR TKI for Patients with EGFRm NSCLC and GBM Selective for mutations versus WT - EGFR to deliver favorable tolerability profile Spares WT - EGFR Oral small molecule with covalent MOA for potency and durability Covalent Designed to treat CNS tumors and brain metastases Brain - Penetrant Phase 2 ongoing in both recurrent and frontline EGFRm NSCLC; Phase 0/1b in frontline GBM Robust clinical activity

8 Evolution of the EGFR mutation landscape over the past 20 years NGS revolution Mutation specific sequencing 2005 (2/3L) 2013 2015 2018 2024 T790M resistance C797S resistance Non - classical drivers Classical drivers L858R / Ex19del R ealization of EGFR non - classical mutations (NCMs) Treatments Sequencing practices Classical EGFR mutations described Mutation landscape BDTX - 1535: opportunity to address unmet need for non - classical drivers and C797S resistance mutations BDTX - 1535 (1L) (2L) (1L) The EGFR Mutational Landscape in NSCLC has Evolved, Revealing a Broad Spectrum of Unaddressed Non - Classical Oncogenic Driver & Drug Resistance EGFR Mutations BDTX - 1535 (1/2/3L)

9 23 - 30% of newly diagnosed EGFRm NSCLC express non - classical mutations Classical and non - classical driver mutations are d istributed across EGFR structure 23 - 30% of Newly Diagnosed EGFRm NSCLC Patients Carry Non - Classical Mutations (NCMs); Not Adequately Addressed by Current Therapies 1. Borgeaud M. JTO 2024 2. Robichaux J, Nature 2021 Dardenne et al AACR 2024 and Heymach et al ESMO 2024 Black Diamond Therapeutics analyses of 94,939 sequencing reports from treatment naïve NSCLC Non - Classical Classical: L858R and Exon19del Adapted from Du et al. 2023. Analysis of the AACR GENIE database of 22,050 cases of NSCLC 23% 30% Ectodomain - Juxtamembrane (non - classical) PACC 2 & others (non - classical) 50+ mutations 60+ mutations R108X R222X A289X C598X S645X … E709X G719X T725M L754E L747X S768I V769X L861X L833X … Current therapies do not adequately address non - classical EGFR mutations 1

CONFIDENTIAL | 10 Heymach et al ESMO 2024 Real World Treatment Data Highlights Significant Unmet Need for Patients with Newly Diagnosed EGFR - NCM NSCLC 0 20 40 60 80 100 % of Patients Treated Afatinib Chemo+/ - I/O Osimertinib Afatinib Afatinib: 8.0 months Chemo +/ - I/O: 4.2 months Time (Months) Time on Treatment (Survival Probability) 0.0 0.2 0.4 0.6 0.8 1.0 15 11 11 20 4 6 Osimertinib 0 90 104 5 54 38 Osimertinib: 6.0 months 10 27 19 Chemo +/ - I/O 20 14 325 95 44 Afatinib: 16.7% Chemo +/ - I/O: 60.1% Osimertinib: 19.4% Chemotherapy used in ~60% of 1L patients, with osimertinib and afatinib used for the remainder Median time on treatment for 1L NCM NSCLC is < 8 months

CONFIDENTIAL | 11 * GuardantInform data derived from collaboration with Guardant Health – data on file at BDTX. UNICORN - 2024: Okuma et al JAMA Oncology 2024. UNI CORN - 2023: Bar et al JTO 2023. ARTICUNO: Pizzutilo et al ESMO Open 2024, mPFS for all NCM represents data for Group A TKI naïve patients, mPFS for other NCMs is for n=27 patients, for whom all but 2 were TKI - naive. FLAURA: Soria et al NEJM 2018. Afatinib mPFS from ACHILLES Sato et al ASCO 2024. mo = months Afatinib mPFS Osimertinib mPFS Mutation Type ARTICUNO (2024) 7.0 mo (n=55) All NCM 9.4 mo (n=40) 9.5 mo (n=44) 5.1 mo (n=20) G719X 3 NCMs in afatinib label 9.4 mo (n=10) S768I 16.0 mo (n=12) L861Q 8.6 mo (n=6) ARTICUNO (2024) 4.0 mo (n =27) FLAURA 14.4 mo L858R Classical mutations 21.4 mo Ex19del >100 unique EGFR - NCMs * Osimertinib and afatinib deliver limited PFS benefit to TKI - naive patients with NCMs other NCMs High Unmet Medical Need for Newly Diagnosed EGFR - NCM NSCLC Patients as Evidenced by Shorter mPFS Compared to Classical Mutation Patients UNICORN (2024) UNICORN (2024) UNICORN (2023) mPFS >12 mo and ORR >50% in 1L EGFR - NCM NSCLC would be clear win for BDTX - 1535 vs current therapies L861Q (12%) S768I (11%) G719X (16%) other NCMs (61%) >100 unique oncogenic mutations Frontline cohort of BDTX - 1535 Ph2 trial enrolling patients with a broad spectrum of NCMs similar to distribution above

12 200mg PK data from Phase 1 dose escalation trial* 1 00mg BDTX - 1535 Achieves Coverage of the EGFR Mutation Spectrum at the Well - Tolerated Oral Dose of 200mg QD * Cmax doses plotted for human PK. PK d ata adapted from poster at EORTC/AACR/NCI International Conference on Molecular Targets and Cancer Therapeutics, October 202 3 Dardenne et al AACR 2024 W T L 8 5 8 R E x 1 9 d e l E x 1 9 d e l + S 7 6 8 I ​ L 8 5 8 R + A 8 5 9 S L 8 5 8 R + A 2 8 9 V L 8 5 8 R + L 6 2 R L 8 5 8 R + E G F R v I I I ​ L 8 5 8 R + G 5 9 8 V L 8 5 8 R + S 7 8 4 F ​ L 8 5 8 R + S 7 8 4 S L 8 5 8 R + E 7 0 9 K L 8 5 8 R + E 7 0 9 V L 8 5 8 R + R 1 0 8 K L 8 5 8 R + V 8 3 4 L K 7 5 4 E ​ L 8 3 3 V ​ T 7 2 5 M ​ A 7 6 3 i n s L Q E A ​ S 8 1 1 F ​ L 8 6 1 Q ​ L 8 6 1 R ​ A 7 6 3 i n s F Q E A ​ S 7 8 4 F G 7 1 9 A ​ G 7 1 9 S ​ L 8 3 3 V G 7 2 4 S ​ L 7 4 7 P ​ L 7 4 7 S ​ E 7 0 9 K ​ I 7 4 0 d u p I P V A I K ​ R 7 7 6 H ​ E 7 0 9 A ​ E 7 0 9 V ​ E 7 0 9 G ​ S 7 6 8 I ​ V 7 6 9 L ​ V 7 6 9 M ​ E 7 0 9 Q ​ G 7 7 9 F ​ L 8 3 3 F E 7 0 9 - T 7 1 0 d e l i n s D ​ L 7 1 8 Q ​ G 7 1 9 C + S 7 6 8 I L 8 5 8 R + L 7 4 7 S E 7 0 9 A + G 7 1 9 S ​ E 7 0 9 K + G 7 1 9 S ​ S 7 6 8 I + V 7 6 9 L ​ L 8 5 8 R + L 7 1 8 V ​ G 7 1 9 A + R 7 7 6 C ​ L 8 5 8 R + S 7 6 8 I ​ L 8 5 8 R + L 7 9 2 H ​ E x 1 9 d e l + L 7 1 8 Q ​ S 7 6 8 I + V 7 7 4 M ​ V 1 0 9 7 I G 7 1 9 C P 7 7 2 L Q 8 1 2 R G 7 1 9 A + R 7 7 6 C G 7 1 9 D D 7 6 1 Y G 7 1 9 R G 7 1 9 A + L 8 6 1 R S 7 2 0 F G 7 7 9 C V 7 7 4 i n s P R I 7 4 4 _ K 7 4 5 i n s K I P V A I ​ R 2 2 2 C R 1 0 8 K A 2 8 9 T E G F R v V I ( D e l 1 2 - 1 3 ) V 6 8 9 M G 5 9 8 V C 5 9 5 S E G F R v V I I ( D e l 1 4 - 1 5 ) C 2 3 1 F S 6 4 5 C A 2 8 9 V E G F R v I I I ( D e l 2 - 8 ) E G F : S e p t 1 4 f u s i o n ​ E x 1 9 d e l + C 7 9 7 S ​ L 8 5 8 R + C 7 9 7 S ​ 0 20 40 60 80 100 120 P r o l i f e r a t i o n ( I C 5 0 ) n M L858R+ Non-Classical Classical-Like P-Loop and αC-Helix Compressing (PACC) Other Non-Classical Ecto- and Juxtamembrane Domain PACC Alone PACC Complex EGFR Non-Classical MutationsClassical EGFR-WT C797S

CONFIDENTIAL | 13 BDTX - 1535 Potently Targets NCMs Which Are Less Sensitive to Osimertinib l oss of potency Osimertinib: weak against most NCMs (most commonly expressed NCMs shown) BDTX - 1535: potent against NCM spectrum (most commonly expressed NCMs shown) Pre - clinical data; EGFR mutations are engineered in Ba/F3 cells BDTX - 1535: potent against NCMs co - expressed with L858R (co - expressed NCMs shown) G719C L858R Ex19del L861Q G719A L747P E709A S768I G719S E709K E709V G719C L858R Ex19del L861Q G719A L747P E709A S768I G719S E709K E709V EGFR mutations frequently associated with L858R

14 Real World Data Demonstrate Frontline L858R Patients Presenting with EGFR - NCMs Discontinue Quickly Following Osimertinib Therapy Poor performance for osimertinib in the context of L858R + NCM NSCLC A spectrum of NCMs co - occur together with L858R EGFR - NCMs frequently p resent as compound m utations together with the classical L858R mutation NCMs more frequently co - occur with L858R vs Ex19del L858R Ex19dels 0 2 4 6 8 10 12 14 % o f c a s e s w i t h E G F R N o n - C l a s s i c a l m u t a t i o n E709X V834L R776X L833X S768I L62R A289X Others T725M R108K 10 15 0.0 0.2 0.4 0.6 0.8 1.0 Ex19del: 14.7 months L858R: 10.8 months 0 1,054 642 62 5 664 360 25 438 217 14 291 130 10 20 185 70 5 L858R + NCM: 5.0 months Time on Treatment (Survival Probability) Time (Months) Heymach et al ESMO 2024

15 BDTX - 1535 Phase 1 Dose Escalation: Summary Mutation Matched Phase 1 Study Inclusion Criteria Once - daily dosing delivers sufficient exposure to inhibit EGFR mutations M anageable EGFR TKI tolerability profile at 200 mg (similar to osimertinib ) Radiographic responses and durable anti - tumor activity across multiple mutation families ctDNA reduction confirms loss of mutant alleles, which is predictive of clinical benefit 1 Data at EORTC 2023 Ph 1 NSCLC Key Data T akeaways • Primary objective: PK and safety • Secondary objective: Anti - tumor activity Dose Escalation Completed: 15 mg QD to 400 mg QD 15 mg QD 25 mg QD 50 mg QD 100 mg QD 200 mg QD 300 mg QD 400 mg QD Recurrent GBM Cohort EGFR alterations at resection/diagnosis Wild - type isocitrate dehydrogenase (IDH) Recurrent NSCLC Cohort EGFR mutations at the time of progression: – Non - classical driver, OR – Acquired resistance C797S Progression after EGFR TKI Exclusion of EGFR T790M, Ex20ins, KRAS mutations, cMET amplification • Target coverage and clinical activity at ≥ 100 mg, MTD at 300 mg 1. Thompson, JC., et al., British Journal of Cancer, 2023.

16 BDTX - 1535 Preliminary Phase 2 Data in Recurrent Setting Patients with non - classical driver mutations after ≤2 prior lines of therapy with osimertinib as the preferred prior EGFR TKI Patients with acquired resistance C797S after ≤2 prior lines of therapy with osimertinib as the only prior EGFR TKI Cohort 2 (enrollment complete 42 pts ) Cohort 1 (enrollment complete 41 pts ) Patients with non - classical driver mutations and no prior treatment Cohort 3 (up to 40 pts) 1 st Line 2 nd /3 rd Line Initial data on 27 pts reported Sept 2024 Initial data expected Q4 2025

17 In Recurrent EGFRm NSCLC, Patients Most Frequently Present with PACC - NCM and C797S Resistance Mutations Classical mutation Non - classical mutation (including PACC - NCM) C797S Resistance 1 . Rotow JK, et al. Journal of Thoracic Oncology , 2023. Under selective pressure, patients acquire / accumulate EGFR resistance mutations osimertinib therapy PACC - NCMs and C797S are major mechanisms of on - target EGFR resistance in patients post osimertinib 1 Recurrent Newly Diagnosed EGFRm NSCLC Dardenne et al. AACR 2024. Heymach et al. ESMO 2024. Classical Non - classical Exon 20

18 0 10 20 30 40 50 60 70 80 90 100 Rash Diarrhea Stomatitis Weight decr Paronychia Nausea Fatigue Alopecia Vomiting Pruritus BDTX - 1535: Favorable Tolerability Profile Patients Randomized to 200mg Starting Dose Treatment Related Adverse Events (TRAE) ≥ 10% Patients Rash includes rash, rash maculo - papular, rash pustular, dermatitis acneiform. AEs in greater than two patients % of patients (n=20) Grade 1 - 2 Grade 3 Data from June 2024 Data Summary • No grade 3/4 diarrhea • No liver enzyme elevation • No QTc prolongation • 1/20 patient discontinued • 4/20 patients dose reduced No new safety/ tolerability signals observed to date

19 *1 patient had 3 prior lines prior lines of treatment (incl. amivantamab ) BDTX - 1535: 200 mg Patient Demographics and Baseline Characteristics Efficacy evaluable patients (N=27) Baseline Characteristics 62 (41, 82) Age, median (range) 19 (70%) Female 16 (59%) ECOG PS 1 6 (22%) CNS metastases at baseline 9 (33%) Visceral metastases at baseline Prior lines of anticancer treatment* 14 (52%) 12 (44%) 1 2 Mutation Stratification 15 (56%) 12 (44%) Cohort 1 (NCMs) Cohort 2 (C797S) Data from September 23, 2024 disclosure

20 Phase 2: Patient Treatment Summary 8 Response evaluable per protocol 27 3 Efficacy evaluable Patients with PACC - NCMs and/or C797S 22 19 Exclusion criteria mutations ID’d by C1D1 liquid biopsy >1 prior EGFR - targeted therapy 2 3 36% Preliminary ORR 42% Preliminary ORR Patients without on - target resistance mutation Data from September 23, 2024 disclosure

21 -100 -80 -60 -40 -20 0 20 40 60 B e s t % S o D c h a n g e 1015-212 4 BDTX - 1535 Phase 2 Preliminary Waterfall Plot Preliminary ORR 42% in patients w ith PACC - NCM and/or C797S uCR cPR SD uPR uPR cPR cPR SD cPR uPR SD SD SD SD SD SD SD PD Best response 33 41 55 46 40 29 63 71 75 77 24 159 51 46 46 48 89 22 Sum Target Lesion (mm) *Retrospective liquid and tissue biopsy NGS testing; Pt 2118 withdrew consent prior to first scan (see patient in swimmer plo t) O - osimertinib; A - afatinib; C - carboplatin, Cis – cisplatin, Pem - pemetrexed; Pac - paclitaxel; B - bevacizumab; HER3 - Dxd - patritumab deruxtecan ; 2152 2110 2195 2207 2208 2097 2115 2172 2179 2198 2184 2181 2158 2169 2197 2160 2124 2199 Patient ID L858R Ex19del Ex19del L858R L858R E19del L858R L858R Classical mEGFR* G719S S768I L833V L747_A755 delinsSKD V774M S768I L718V G719A S768I Y1016C L747_P753 delinsS L718V G930R G719A S768I L747_A750 delinsP L747_P753 delinsS K745N Ex19Ins - IPVAIK K745N R108K E19delinsD E709A NCM C797S C797S C797S C797S C797S C797S C797S C797S C797S C797S O 8.5 O 50.0 O 15.8 O 14.1 A 13.9 O 38.3 O 24.9 O 5.1 C+pac 1.3 O+B 67.5 Osi 19.0 O+Cis+Pem 1.4 O 23.5 O 22.8 O 20.8 O 25.8 O 1.5 O 19.6 Prior 1L Duration, months C+Pac 1.8 O+C+Pem+ B 26.6 HER3 - Dxd 0.8 O+C+Pem 3.0 Osi 16.8 O+C+Pem 4.0 O+C+Pac 6.9 O+C+Pem 6.4 Prior 2L Duration, months TK/MAPK RTK PI3K MAPK RTK Off - Pathway Detected Cohort 1 - NCM: 4/9 pts w/ responses Cohort 2 - C797S: 4/10 pts w/ responses Remains on therapy Data from September 23, 2024 disclosure

22 0 1 2 3 4 5 6 7 8 9 10 11 26 25 23 22 21 18 17 14 13 12 11 10 9 8 7 6 5 2 1 Months on Treatment P t I D PD SD PR Best response Prior Therapy EGFR Mutation(s) Pt ID 2nd 1st C797S Non - classical Classical cPR Osi+C+pem+bev Osi C797S L833V L858R 2110 cPR HER3 - DXd Osi L718V L858R 2115 uCR C+pac Osi G719S; S768I 2152 SD Osi C797S L747_A750delinsP 2158 SD Osi C797S R108K L858R 2160 cPR* Osi C797S Exon 19del 2097 SD Osi C797S L747_P753delinsS 2169 SD Osi+C+Pem Osi G719A; S768I 2172 cPR Osi C+pac C797S Y1016C L858R 2179 SD Osi+C+pac Osi+C+pem G719A; S768I 2181 SD Osi C797S Exon 19del 2184 SD Osi E709_T710delinsD 2124 SD Osi C797S Exon 19del 2195 SD Osi+pem+C Osi K745_E746insIPVAIK K745N 2197 PD Osi E709A L858R 2199 uPR Osi+C+pem Osi+bev L718V; L747_P753delinsS; G930R 2198 uPR Osi C797S L747_A755delinsSKD 2207 uPR Afatinib V774M; S768I 2208 WC C+pem/CPI Osi C797S L747_T751del ; V834L 2118 Ongoing uCR N=19 in swimmer plot, including Pt 2118 who withdrew consent (WC) prior to first scan *Patient discontinued (pneumonitis) BDTX - 1535 Phase 2 Preliminary Swimmer Plot Encouraging durability with 14 out of 19 patients still on therapy Mean follow - up: 4.7 months Data from September 23, 2024 disclosure

23 Patient 2152: Unconfirmed Complete Response and Remains on Therapy Data from September 23, 2024 disclosure LN= lymph node, SoD = Sum of diameters per RECIST 1.1 Absent Present Pleura Present Absent/Normal Present LN - pleura Present Absent Present Brain Present PR 200 mg PR PR PR Baseline CR Absent Present Brain Present 1 Target Lesion Omentum SoD = 33 mm 5 Non - Target lesions -100.0 -80.0 -60.0 -40.0 -20.0 0.0 20.0 (-1 mo) 1.5 mo 3 mo 4.5 mo 6.0 mo 7.5 mo % SoD change Mutations and Prior Therapies 2 NCMs: G719S and S768I Mutations: 1L osimertinib 8 months 2L carbo/pem 2 months Prior Therapies: Screening C7D1 Absent Present Mesentery Present

24 2179 2110 2097 Patient ID PR PR PR BDTX - 1535 Eradicates EGFRm Alleles and Drives ctDNA Clearance Eradication of targeted variant alleles and reduction of ctDNA are early predictors of PFS 1 -100 -90 -80 -70 -60 -50 -40 -30 -20 -10 0 0 2 4 6 8 C1D1 C3D1 %ctDNA clearance %VAF of EGFRm C797S E746_A750del ctDNA -100 -90 -80 -70 -60 -50 -40 -30 -20 -10 0 0 1 2 3 C1D1 C3D1 %ctDNA clearance %VAF of EGFRm C797S L833V L858R ctDNA -100 -90 -80 -70 -60 -50 -40 -30 -20 -10 0 0 2 4 6 8 C1D1 C3D1 %ctDNA clearance %VAF of EGFRm C797S L858R Y1016C ctDNA Of 8 patients with PRs, ctDNA testing on 3 patients shown above, insufficient DNA on 2 patients, and pending testing on 3 pat ien ts 1. Thompson, JC., et al., British Journal of Cancer, 2023 Data from September 23, 2024 disclosure

25 # includes Ex19del (E746_A750) and L858R; *Includes atypical Ex19dels with variable sensitivity to osimertinib ( Heymach et al ESMO 2024) ^ osimertinib - sensitive mutations (Robichaux et al Nature 2021, Heymach et al ESMO 2024) ; osi = osimertinib C797S Other NCMs* PACC NCMs Classical # Patient ID C797S Exon 19del 2195 C797S Exon 19del 2184 C797S Exon 19del 2097 C797S L833V L858R 2110 C797S R108K L858R 2160 C797S Y1016C L858R 2179 C797S L747_A750delinsP^ 2158 C797S L747_P753delinsS ^ 2169 C797S L747_A755delinsSKD^ 2207 C797S L747_T751del^ ; V834L 2118 L718V L858R 2115 E709A L858R 2199 G719S; S768I 2152 G719A; S768I 2172 G719A; S768I 2181 E709_T710deInsD 2124 K745N K745_E746insIPVAIK 2197 V774M; S768I 2208 L747_P753delinsS^; G930R L718V 2198 L747P_P753delinS^ 2203 L861Q^ 2101 L861R^; L62R 2188 9 pts with PACC - NCMs 10 pts with C797S 3 pts with other NCMs All mutations identified with common practice NGS BDTX - 1535 Phase 2 Clinical Activity Across Broad Spectrum of EGFR Mutations Found in Recurrent Post EGFR TKI Patients Preliminary ORR of 42% in 19 patients with PACC - NCM or C797S mutations Pts w/ PR Data from September 23, 2024 disclosure • Patients with osi - sensitive NCMs without any EGFR resistance mutations. • BDTX - 1535 expected to deliver benefit in patients with these mutations in 1L setting.

26 BDTX - 1535: Key Takeaways from Phase 2 Data in Recurrent NSCLC Patients BDTX - 1535 has a well - tolerated safety profile at 200mg once daily BDTX - 1535 achieves RECIST responses and shows promising initial durability across patients presenting with a broad - range of non - classical mutations including PACC and C797S BDTX - 1535 achieves RECIST responses in brain metastases BDTX - 1535 has also demonstrated brain penetrance in a Phase 0/1 trial in of patients with recurrent GBM Data in recurrent NSCLC patients highlight favorable properties for continued development in newly - diagnosed patients with NCMs

27 BDTX - 1535 Phase 2 Status Patients with non - classical driver mutations after ≤2 prior lines of therapy with osimertinib as the preferred prior EGFR TKI Patients with acquired resistance C797S after ≤2 prior lines of therapy with osimertinib as the only prior EGFR TKI Cohort 2 (enrollment complete 42 pts) Cohort 1 (enrollment complete 41 pts) Patients with non - classical driver mutations and no prior treatment Cohort 3 (up to 40 pts) 1 st Line 2 nd /3 rd Line Final data expected H1 2026 Initial data expected Q 4 2025

28 Ami: Amivantamab Laz: Lazertinib 1 st line Locally advanced/metastatic EGFRm NSCLC 2 nd line 3 rd line Platinum Doublet +/ - Ami Platinum Doublet Docetaxel Docetaxel Osimertinib +/ - Platinum Doublet Ami + Laz Afatinib FDA label for 3 NCM Platinum Doublet Osimertinib NCCN Only Classical EGFRm Non - classical EGFRm On Target Progression via EGFR Mutations (e.g., C797S, PACC - NCMs) BDTX - 1535 1L NCMs BDTX - 1535 Recurrent (2L+) Current Treatment Landscape for EGFRm NSCLC

29 Infusion - based regimens BDTX - 1535 monotherapy Intravenous Route of administration Oral once daily High rates of grade 3 AEs Safety and tolerability Generally well - tolerated Classical Mutation coverage Classical + non - classical Burdensome Patient QoL Opportunity for high QoL for year(s) BDTX - 1535: Well - Positioned for Success in Frontline EGFR - NCM NSCLC No head - to - head study has been conducted between BDTX - 1535 monotherapy and chemo - based combination regimens.

30 BDTX - 1535: Broad Potential to Benefit EGFRm NSCLC Patients Across Multiple Lines of Therapy 1L non - classical mutations Recurrent setting with EGFR - resistance mutations Adjuvant/post - adjuvant 1L L858R (+) Topline Ph2 results Sept’24 Potential for longer duration of therapy, including: • Non - classical adjuvant setting • 1L patients with EGFR - resistance mutations post - adjuvant osimertinib Highly potent vs. L858R alone and co - expressed non - classical mutations Targeting OS benefit in EGFR L858R NSCLC ~5,000 – 11,000 ~18,000 – 22,000 ~7,000 – 14,000 ~27,000 – 30,000 Estimated Addressable Patients in G7 Countries Phase 2 initial data expected Q4 2025 Anticipate FDA feedback on approval pathway Q4 2025 Data Monitor Pharma Intelligence; Zhang Oncotarget 2016; Heymach ESMO 2024; Kantar Treatment Architecture; Rotow JTO 2023; BDTX Internal Data Analysis; Foundation Med AACR 2023; Bertoli Int J Mol Sci 2019; Piotrowska Annals of Oncology 2022

31 BDTX - 1535: Opportunity in Glioblastoma

32 1. Saadeh, F., et al., The International Journal of Biological Markers, 2018 2. Real world evidence data from Tempus Labs a nal ysis of 2,540 GBM patient samples Treatment of EGFR - Driven GBM Requires Inhibition of Complex EGFR Mutations: Potent Preclinical Inhibition by BDTX - 1535 Of all ECD - driven tumors were complex, containing 2 or more ECD mutations Of complex ECD - driven tumors were highly heterogeneous, with 3 or more ECD mutations 12% 2 40% 2 32% 2 52% 1 Of all GBM samples had EGFR extracellular - domain (ECD) mutations, according to real - world evidence Of all GBM samples carry oncogenic EGFR alterations GBM patients in the US are diagnosed each year with EGFR mutations that have been shown in preclinical studies to be inhibited by BDTX - 1535 ~7,000

33 BDTX - 1535: Potential to Overcome Limitations of Prior Attempts to Drug EGFR in GBM Lessons From Past Failures BDTX - 1535 MOA=mechanism of action; CNS=Central Nervous System; WT=Wild - Type; GBM=Glioblastoma Multiforme; NSCLC=Non - Small Cell Lung Cancer Potent MasterKey inhibition of co - occurring EGFR alterations and amplification Heterogenic expression of EGFR oncogenic alterations within tumors Covalent MOA and no paradoxical activation Paradoxical activation of EGFR GBM oncogenes induced by reversible inhibitors Spares WT - EGFR in normal cells while retaining potent activity against EGFR alterations Poor tolerability driven by on target WT - EGFR activity Brain - penetrant to treat CNS tumors Low brain exposure due to a lack of CNS penetrance

34 Encouraging Data for BDTX - 1535 in the Recurrent Setting; Initiating Phase 0/1b Trial in Newly Diagnosed GBM Patients Wen et al ASCO 2024, Sanai et al ASCO 2024, Sanai et al EANO 2024, Sanai et al SNO 2024, and Sanai et al AACR 2025 Ph 1 Dose Escalation in 2L+ ▪ 27 patients with recurrent disease ▪ Generally well tolerated @ 200mg ▪ Preliminary efficacy Confirmed safety Data at ASCO 2024 Initial data expected Q2 2026 Preliminary survival ▪ Up to 48 newly diagnosed patients ▪ Pre/post treatment biopsies (Ph 0) ▪ Treatment phase (Ph 1b) Phase 0/1b in 1L Data at ASCO/EANO/SNO 2024 and AACR 2025 Confirmed brain exposure ▪ 22 patients with recurrent disease ▪ Demonstrated brain exposure ▪ P reliminary PD/efficacy Phase 0/1 in 2L+ Encouraging clinical activity in recurrent setting

CONFIDENTIAL | 35 Phase 0/1 Trial in Recurrent GBM Patients: BDTX - 1535 Exceeds Targeted Exposure in Non - Contrast Enhancing Regions of Brain Tumors Sanai et al SNO 2024. NE = non - enhancing, E = enhancing, CSF = cerebral spinal fluid Exposure in GBM tumors exceeds IC50 for targeted mutations Decreased pEGFR vs. pretreatment archival tissue phosphoEGFR

CONFIDENTIAL | 36 Phase 0/1b IST in Newly Diagnosed GBM Patients: Potential to Deliver Data to Guide Future Registrational Study Phase 0/1b study: enrolling up to 48 patients with confirmed presence of EGFR alterations BDTX - 1535 as monotherapy for 5 days prior to resection Days 1 - 5 Newly diagnosed GBM patients Confirmation of EGFR alteration (needle biopsy) BDTX - 1535 + RT 6 - 7 weeks BDTX - 1535 monotherapy 28 - day cycle until PD PK / PD Surgical resection

37 BDTX - 1535: Anticipated Milestones Q2 2025 – 1H 2026 Final Phase 2 results 2Q25 3Q25 4Q25 1H26 1L NSCLC GBM 2L /3L NSCLC Financial Summary as of December 31, 2024 Servier upfront for BDTX - 4933 Cash runway into Q4 2027 Phase 0/1 data in recurrent patients at AACR (IST at Ivy) Initial Phase 2 results and FDA feedback on approval pathway Initial Phase 0/1b data in newly diagnosed patients (IST at Ivy) $98.6 M + $70M

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