Transforming and Innovating the Discovery and Development of Novel, Class Leading GPCR-Targeted TherapiesJ u n e 2 0 2 4 Transforming and Innovating the Discovery and Development of Novel, Class Leading GPCR-Targeted The

Transforming and Innovating the Discovery and Development of Novel, Class Leading GPCR-Targeted TherapiesJ

Transforming and Innovating the Discovery and Development of Novel, Class Leading GPCR-Targeted TherapiesJ

u n e 2 0 2 4DISCLAIMERStatements contained in this presentation regarding matters that are not historical facts are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Words

such as anticipates, believes, expects, intends, plans, potential, projects, would and future or similar expressions are intended to identify

forward-looking statements. Each of these forward-looking statements involves substantial risks and uncertainties that could cause actual results to differ significantly from those expressed or implied by such forward-looking statements.

Forward-looking statements contained in this presentation include, but are not limited to, statements regarding: the design, objectives, initiation, timing, progress and results of current and future preclinical studies and clinical trials of our

product candidates, including the ongoing Phase 1a/b clinical trial for TX45, in Group 2 Pulmonary Hypertension and initiation of proposed Phase 2 clinical trial; candidate selection for our second program in HHT; the expected timing of program

updates and data disclosures; the timing of filing INDs and other regulatory documents; the timing and likelihood of seeking regulatory approval for our product candidates including TX45; the competitive landscape for our product candidates; our

ability to identify and develop additional product candidates; and our estimates regarding expenses, future revenue, capital requirements, cash runway and needs for additional financing. These forward-looking statements reflect our current beliefs

and expectations. Many factors may cause differences between current expectations and actual results, including the early stage of our development efforts; success in preclinical testing and earlier clinical trials does not ensure that later

clinical trials will generate the same results or otherwise provide adequate data to demonstrate the efficacy and safety of a product candidates; clinical site activation rates or clinical trial enrollment rates that are lower than expected; changes

in expected or existing competition; changes in the regulatory environment; the uncertainties and timing of the regulatory approval process; the impact of macroeconomic conditions, including the conflict in Ukraine and the conflict in the Middle

East, heightened inflation and uncertain credit and financial markets, on our business, clinical trials and financial position; and unexpected litigation or other disputes. These and other risks are described more fully in our filings with

theSecurities and Exchange Commission ( SEC ), including the risks detailed in the prospectus filed with the SEC pursuant to Rule 424(b)(3) on May 3,2024, and other documents we subsequently filed with or furnished to the SEC. All

forward-looking statements contained in this presentation speak only as of the date on which they were made. Except as required by law, we assume no obligation to update any forward-looking statements contained herein to reflect any change in

expectations, even as new information becomes available. This presentation also contains estimates and other statistical data made by independent parties and by us relating to market size and growth 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 estimates. Neither we nor any other person makes any representation as to the accuracy or completeness of such data or undertakes any obligation

to update such data after the date of this presentation. 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 high degree of

uncertainty and risk.

AgendaI. Company OverviewII. GEODeTM PlatformIII. TX45 Relaxin in Group 2 Pulmonary Hypertension i. Overview of

Target and Indication ii. Patient Journey iii. Clinical Data iv. Preclinical Data v. Clinical ProgramIV. HHT Program V. Summary

Agenda I. Company Overview II. GEODeTM Platform III. TX45 Relaxin in Group 2 Pulmonary Hypertension i. Overview

of Target and Indication ii. Patient Journey iii. Clinical Data iv. Preclinical Data v. Clinical Program IV. HHT Program V. Summary4 Tectonic Therapeutic Transforming the Discovery of Novel GPCR-Targeted Therapies, Innovating in Their

Development Validated GEODe Validated platform to discover and optimize biologics that target GPCRsPlatform Prioritizing high value GPCR targets, where small molecules are not the right modality First two assets address indications with no approved

therapy 1. RXFP1 agonist potential therapy for Group 2 PH1 in HFpEF2 >600,000 Patients in US alone (>20 times PAH) Phase 1 Best-In-ClassRelaxin Agonist for

PH, Initial Phase 1a PK/PD data demonstrated activity and favorable PK with potential for monthly dosing; full data mid-2024

First-In-Class HHT Phase 1b hemodynamic proof of concept expected in 2025, randomized Phase 2 data Program expected in 2026 2. GPCR antagonist antibody addressing

hereditary hemorrhagic telangiectasia(HHT)Team with a Track Team with extensive track record of drug discovery and development success,Record of Firsts resulting in 20 first approvals across multiple therapeutic areas Reverse

Merger Closed Well capitalized by a syndicate of leading institutional funds June 2024 $181M3 post close expected to provide runway into mid-2027 1Pulmonary Hypertension; 2Heart Failure with Preserved Ejection

Fraction; 3At transaction close (6/20/24), cash, cash equivalents and investments of approximately $181 million, before payment of final transaction-related expenses, is expected to fund current operational plans into mid-2027

This Accomplished Team Has Delivered for Patients and Investors Reicin, M.D. Lochner McNamara, Ph.D. Muslin,

M.D. Ruddy, M.D. Schwabish, Ph.D. CEO, Director CFO CSO CDO CMO CBO FOUNDED MULTIPLE GPCR EXPERT, SUCCESSFUL COMPANIES FORBES 30 under 30 Timothy AndrewSpringer, Ph.D. LeukoSite Kruse, Ph.D.Co-Founder

Co-Founder Multiple Awards and Fellowships 2022 Lasker Award (Biomedical Research, NIH, Amgen, Sloan Research)

Team Track Record: >20 1st Approvals with >$50B In Annual Sales 1st approvals and indication expansions

shown below ONCOLOGY/ IMMUNOLOGY/ CARDIO/ RESPIRATORY OTHER IO INFLAMMATION METABOLISM / ALLERGY

Biologics Offer Advantages Over Small Molecules in Targeting GPCRs in Multiple Settings ~12%

>18%*Approveddrugs target remain When difficult to drug with small molecules 100 GPCRs unexploited Biologic captures complexity of ligand / receptor engagement If target site similar to domains of different proteins Biologic minimizes off target

binding to improve safety / tolerability 800+ Non- Sensory GPCRs Orphan If use case requires tissue /compartment targeting GPCRs Sensory (~20%) Engineer biologic to target or exclude compartment as needed

GPCRs (~50%) When multi-modal action neededBispecific approach enables dual target engagement >470 Approved drugs (~33% of all) >$180B in annual sales Predominantly small molecules Only 3 are antibodies (*) Hauser, A.S. et al., Cell. 2018 Jan

11; 172(1-2): 41 54.e19. * 18% = 100% 12% (approved drug targets) 50% (sensory) 20% (non-sensory, orphan)

Our Unique Pipeline Opportunities are Enabled by Biologic Targeting of GPCRs GRO RY HEREDITARY HYPERTENSION

(Group 2 PH) TELANGIECTASIA (HHT) First in Class & Indication Bi-specific Approach Potential Best-in-Class GPCR

Antagonist2 GPCR Modulator2 RXFP1 Agonist1 (anti-angiogenic) (anti-fibrotic) Supporting clinical data Target pathway linked to disease Supporting clinical data for one genetics component of bispecific Scale of POC studies: ~50-200 patients per indication 3-6 months treatment 1. Fusion protein lead molecule in-licensed from Harvard U., optimized

using GEODe platform 2. GPCR targeted therapeutics discovered internally using GEODe platform

Pipeline of GPCR-Targeted Biologics with Multiple Potential Value Infection Points Ahead Development programs

include first-in-indication opportunities*Program Preclinical Phase 1 Phase 2 Phase 3 Indication * Group 2 PH(1) in Phase 1a (ongoing) Initiation Planned Patients with

HeartRXFP1 AgonistPK/PD data mid-2024 2H 2024 Failure with(TX45 Fc-relaxin)Phase 1b (ongoing) Randomized Hemodynamic data 2025Phase 2 Data 2026 Preserved

EjectionFraction (HFpEF) * Hereditary GPCR DevelopmentInitiation Hemorrhagic CandidatePlanned Telangiectasia Antagonist Selection Q4 25/Q1 26 (Osler Weber Rendu Syndrome) Bi-functionalDiscovery

Fibrosis GPCR Modulator GPCR MultipleDiscovery Modulators Indications (1) Pulmonary Hypertension

GEODe PLATFORM Proprietary, validated platform, enables reproducible discovery and optimization of GPCR

11 Solving Key Challenges in GPCR Targeted Biologics Discovery GEODe Platform Features Challenges Designed for

Success RETAIN 1.endogenous GPCR structure to enable screening against relevant form of receptor Receptor Engineering, and Purification Technologydelivers abundant receptor reagent in native conformation PURIFY target in sufficient quantities to

power screening campaign 2.In-vitro Yeast Display Libraries INDUCE provide high-diversity, without immune editing immune response to human GPCR in animals if immunization strategy is pursued 3.STABILIZE

Protein Engineering receptor in active conformation to enable Optimize protein pharmacologyagonist discovery Engineer antigen formats to enable screening for agonists or antagonists as needed

Proprietary GEOD platform spans three enabling technologies to identify and optimize potent GPCR targeted

biologics 1. 2. 3.EXPRESSION AND IN-VITRO YEAST PROTEIN ENGINEERING PURIFICATION TECHNOLOGY DISPLAY LIBRARIES Produce Sufficient Quantities Efficiently Screen Optimize Protein Pharmacology and Stabilize Them

in the Diverse Antibody Libraries Engineer Proprietary Scaffolds Correct Conformation Against GPCRs for Agonist Discovery Large toolbox of biochemical methods, engineering tools, and assays

GEODe 13 GEOD Platform Discovery Capabilities Deliver Selective, Ligand Competitive Orthosteric Antagonists

PURIFIED ANTIBODIES ARE OPTIMIZATION IMPROVES SELECTIVEFUNCTIONAL ANTAGONISTS* ORIGINAL POTENCY BY ~20X (NO EFFECT ON OFF-TARGET GPCR) Receptor Signaling Assay (Mammalian Cells) assay) 125assay) X786 200 Hit

Optimized Lead 100 X774 y 150 arrestin it ity v i 75 arrestin - v t 100 Ac 50 %Act % 50 (+) Ctrl Optimized Lead (hGPCR3 25(hGPCR2 0 Activity 0V Activity V % -11 -10 -9 -8 -7 -6 -5% -12-11-10 -9 -8 -7 -6 -5 -4 Log[Antagonist], M Log[Antagonist], M *Latest generation proprietary libraries delivering initial hits with >10X potency

GEODe 14 Our Proprietary Antigen Formats Enable Screening for Biologics with Agonist Activity Active Inactive

GPCR GPCR Membrane Proprietary Ga Mimetics Designs Driven by Machine Cytosol Learning and Energy Prediction Algorithms ProprietaryG mimetic

Design of Our Proprietary G Mimetics Is Driven by the Latest in Machine Learning and Energy Prediction

Algorithms Nucleotide-bound In-silico Deep Mutational Mutations Predicted to Stabilize the Confirmation Scanning for Receptor-bound GPCR Bound Conformation of G Stabilizing Mutations and Increase Agonist

Affinity 5 (CTH) Nucleotide-bound structures Helical Domain GTPa1 Domain Receptor-boundConfirmation GPCR GPCR-bound GPCR + structures Gs mimeticBinding maximum) (CTRL) (% Candidate mutation log [agonist] M Competition binding assay Ongoing

enhancement of our ability to screen for biologics with agonist activity

Capabilities in Place at Tectonic for Continued Discovery of Optimal DCs Suite of Ab Discovery, Optimization and Characterization Capabilities Target Prep for GPCR structural and mechanistic know-how TARGET

GPCR Biochemistry Overexpression & stabilization of target Discovery Campaigns Mammalian and insect cell expression methods Affinity Maturation Antibody yeast display VALIDATED Antibody Discovery Custom selection methods for GPCRtargets

Protein Engineering HIT NGS to identify diverse sequences High throughput antibody expression DevelopabilityProtein Sciences Biochemical binding Assays Assessment Biophysical characterization LEAD Functional Signaling and cell biology assays to

validateCellular Structural Assessment / lead functionality Pharmacology Biology Structural Cryo-EM of Ab/receptor complex to gain key Insights mechanistic insights, understand SAR DC Candidate In vivo

Disease-specific cell assays Disease Biology Selection Pharmacology PK and animal models

TX45: Fc-RELAXIN FUSION PROTEIN RXFP1 agonist with differentiated

Hemodynamic and Anti-fibrotic Properties of Relaxin Demonstrated by its Role in Pregnancy Pharmacology

Facilitates Gestation AGONIST PULMONARY AND SYSTEMIC VASODILATOR Natural Ligand of RXFP1 Increases cardiac output to Receptor accommodate the increased demand from developing fetus No RXFP1 internalizationANTIFIBROTIC Prepares musculoskeletal

tissues for pregnancy and childbirth

The First Recombinant Relaxin (serelaxin) Demonstrated Safety and Benefit in Acute Heart Failure (AHF) in

Trials of >11,000 Patients -Note: trials only included a two-day relaxin infusion Study (WHF Day 5) Relative Risk [95% CI] N(drug) N(pbo) PK limitations of relaxin

aPre-RELAX AHF 0.56 [0.22 1.45] 42 61 major hurdle to itsRELAX-AHF 0.54 [0.37 0.78] 581 580 development for chronic diseases

RELAX-AHF-2 0.90 [0.76 1.07] 3274 3271 RELAX-AHF-EU 0.71 [0.52 0.98] 1756

894 RELAX-AHF-ASIA 0.42 [0.21 0.84] 437 433 Our GEODe Protein Engineering capabilities0.77 [0.67 0.89] Meta Analysis 6090* 5239 address this challenge p =

0.0002 Effects of serelaxin on worsening heart failure (WHF) fixed-effect (FE) meta-analysis; serelaxiday vs. placebo,. CI, confidence interval. One of two pivotal studies included in meta-analysis, RELAX-AHF-2, failed to achieve the co-primary endpoints, and we believe that two factors contributed to this outcome It was ambitious to expect that a two-day infusion of serelaxin, with its short half-life and mechanism of action, would demonstrate clinical benefit at day 5 and, more puzzlingly at 6 months Operational challenges with patient enrollment may

also have had an impact Teerlink J.R. et al. Eur. J. Heart Fail. 2019; 22: 315-329; patients from RELAX-AHF-JP (N=30 total) not

TX45 is Engineered to Solve a Critical PK Problem Observed with Other Relaxin Molecules TX45 EXHIBITS SUPERIOR

PROFILE vs. PARENT COMPOUND AND COMPARATOR2 MOLECULE3 Preclinical Rat Pharmacokinetic Data Relaxin has very short in vivo half-life Fc-fusion needed to improve PKRelaxin

Fc-fusions have steep decline in exposure after dosing (>90%) because of pI <9, TX-45 glycocalyx binding due to high pI1 pI >9, Comparator Concentration pI

>9, TX early Engineering TX45 to reduce net positive charge (and lower pI) prevents rapid clearance1. Isoelectric Point 2. High pI Fc-relaxin fusion protein described in literature 3. Source: Tectonic

TX45 Reflects Significant Protein Engineering to Optimize Its Pharmacology TX45 results in ~10x greater in vivo

potency over comparator1 molecule than predicted based on PK and in vitro activity2 potentially from reduced trapping of drug in glycocalyx, resulting in increased free drug available to activate RXFP1 in tissuesSuperior efficacy (Renal Blood

Flow) in TX45 vs.Relative in Relative in Expected in Observed inHigh PI Comparator Molecule at Same Dose3 vivo exposure vitro potency vivo activity at vivo activity at at same dose on receptor same dose same dose 1X 10X 10X 1X 10X 10X 1X 10X TX45

0.3mpk TX45 0.03 mpk Comparator 0.3 mpk Vehicle Comp TX45 Comp TX45 Comp TX45 Comp TX45 1. High pI Fc-relaxin fusion protein described in literature 2. ~0.03 mpk of TX45 has similar efficacy as 0.3 mpk of

Comparator 3. Source: Tectonic internal data

TX45 Optimized RXFP1 Agonist for Group 2 PH in HFpEF Potential Best-in-Class Relaxin Protein engineering has extended pharmacologic half-life toAgonist with Optimized PK support monthly dosing HighNeed in No approved therapy Unmet Group 2 >600,000 patients in USPH

with HFpEF1 High 5-year high mortality Mechanism may be Ideal to Pulmonary + systemic vasodilation, cardiac relaxation Reversal of fibrosis in pulmonary vasculature and heart Address Group 2 PH Anti-

inflammatory Supporting Clinical and Pre- Hemodynamic benefit in studies of serelaxin in AHF clinical Data Clear benefit observed with TX45 in rodent PH and CHF models Streamlined Development No outcome study

needed Enrichment strategy for CpcPH where there is greatest unmet need Strategy Enables potential early launch relative toheart failure congestive Potential to Expand Indications Other PH Groups, Heart failure, renal disease1. Heart Failure with

preserved Ejection Fraction

Pulmonary Hypertension Consists of 5 Distinct Diseases Group 2 PH is of Greatest Interest for TX45 s

Initial Indication Group 1Group 2 Group 4 Group 5( PAH ) 1 Group 3 1 (>600,000 ) ( CTEPH ) (Misc.) (~25,000 ) Idiopathic Due to left heart Due to lung disease Chronic thrombo- Miscellaneous disease (HFpEF, or hypoxia embolic

pulmonary group with causes Hereditary HFrEF) or valvular hypertension i.e., unclear or multiple heart disease May be due to as a consequence underlying factors Connective tissue COPD, interstitial of blood clots disease-associated CAD, HTN,

T2DM2, lung disease (i.e., high cholesterol are IPF) or obstructive Congenital heart risk factors sleep apnea disease-associated Two Subtypes: Drug-induced CpcPH / IpcPH 1. US Prevalence 2. CAD: Coronary Artery Disease, HTN: Hypertension, T2DM: Type