1 Corporate Presentation: May 2024 NASDAQ: CDTX

2 Fo r w a rd - L o o k i n g S ta t e m e n t s T h e s e s l i d e s c o n t a i n f o r w a r d - l o o k i n g s t a t e m e n t s w i t h i n t h e m e a n i n g o f t h e P r i v a t e S e c u r i t i e s L i t i g a t i o n R e f o r m A c t o f 1 9 9 5 . The words “may,” “will,” “estimate,” “plan”, “anticipate,” “expect,” “potential,” “could,” “project,” and similar expressions (including the negative thereof), are intended to identify forward-looking statements. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Such statements include, but are not limited to, statements regarding Cidara’s research and development efforts; preclinical and clinical development activities; plans, projections and expectations for and the potential effectiveness, safety and benefits of, its product candidates, including CD388, CBO421 and other antiviral and oncology product candidates from the Cloudbreak platform; whether CD388 may have significant advantages beyond and in addition to flu vaccines; and advancement of its strategic plans Additional risks and uncertainties may emerge from time to time, and it is not possible for Cidara’s management to predict all risk factors and uncertainties. Cidara cautions that the foregoing list of factors is not exclusive and not to place undue reliance upon any forward-looking statements which speak only as of the date of this presentation. Except as required by law, Cidara does not undertake any obligation to update publicly any forward- looking statements for any reason after the date of this presentation to conform these statements to actual results or to changes in its expectations. Projections, assumptions and estimates of the future performance of the markets in which Cidara operates are necessarily subject to a high degree of uncertainty and risk, including, Cidara's ability to obtain additional financing; the success and timing of Cidara’s preclinical studies, clinical trials and other research and development activities; receipt of necessary regulatory approvals for development, as well as changes to applicable regulatory laws in the United States and foreign countries; changes in Cidara's plans to develop its product candidates; Cidara's ability to obtain and maintain intellectual property protection for its product candidates; and the loss of key scientific or management personnel. These and other risks and uncertainties are described more fully in Cidara's Annual Report on Form 10-K for the fiscal year ended December 31, 2023 filed with the United States Securities and Exchange Commission ("SEC“’) on April 22, 2024, and in Cidara’s other filings with the SEC.

3 C D 3 8 8 Re a c q u i re d f ro m J a n s s e n P h a r m a c e u t i c a l s

4 Re za f u n g i n D i v e s t e d t o M u n d i p h a r m a * Cost savings to be applied to advancing CD388 and other Cloudbreak development programs, including CBO421 $67M $61M Approximately $67M in clinical development and CMC costs over next three years Approximately $61M in forecasted obligations through the patent life of rezafungin *Napp Pharmaceutical Group, an affiliate of Mundipharma. Total Estimated Cost Savings: $128M

5 CLOUDBREAK T h e N e w C i d a ra – C l o u d b r e a k ® D r u g F c C o n j u g a t e ( D F C ) P ro g ra m s Program Indication Discovery Preclinical IND-enab. Phase 1 Phase 2 Viral Neuraminidase Prevention of Seasonal Influenza CD73 Solid Tumors, TNBC1 PD-1/ CD73 Solid Tumors CCR5 Solid Tumors Note: Additional programs in preclinical development not disclosed CD388 CBO421 • CD388; Phase 2a completed • CD73 development candidate • Dual inhibitor program • Chemokine receptor program 1. TNBC = Triple Negative Breast Cancer

6 C l o u d b re a k D F C s : A M o d u l a r P l a t fo r m W i t h B ro a d A p p l i c a t i o n s A c ro s s M u l t i p l e T h e ra p e u t i c A re a s DRUG Fc CONJUGATE (DFC) Small molecule Targeting Moiety (TM) All the strengths of mAbs with several potential advantages • Efficient targeting of cryptic sites and small molecule receptors • Tunable valency to exploit avidity for improved potency • Multiple routes to low molecular weight multispecific agents Non-cleavable linker No intracellular exposure = Superior safety vs small molecule drugs • Greater freedom to optimize TMs for target potency • Potential to inhibit “undruggable” targets Proprietary hIgG1 CH1-Fc hybrid domain Multiple tunable attributes • Immune effector function • Half-life extension 2.5x smaller than mAbs • Superior tissue/tumor penetration A u n i q u e l y t u n a b l e p l a t f o r m t h a t c o m b i n e s a n d e x p a n d s u p o n t h e s t r e n g t h s o f s m a l l m o l e c u l e ( S M ) a n d a n t i b o d y t h e r a p e u t i c s mAbs = Monoclonal Antibodies

7 D F C s M ay I m p ro v e S m a l l M o l e c u l e D r u g Po t e n c y a n d S a fe t y DFC Target Cell Target Cell Cyp450s, intracellular proteins Multivalent target engagement increases potency, reduces resistance potential Unlike most small molecules, DFCs don’t enter cells, reducing off-target risks, DDIs DFC DFC DDIs = Drug-drug Interactions

8 % hERG inhibition @10mM SM 77 DFC < 5 D F C s H av e Re d u c e d Po t e n t i a l fo r O f f - Ta rg e t Tox i c i t y Many SM programs have failed to advance due to intracellular off-target toxicity (e.g., hepatotoxicity)* Cardiovascular toxicity due to hERG inhibition has impaired clinical development in many SM programs* Target Cell Cyp450s, intracellular proteins DFC D F C s c a n e x p l o i t d r u g t a r g e t s t h a t a r e d i f f i c u l t t o d r u g w i t h s m a l l m o l e c u l e s ( S M s ) *Kim, et. Al., “CCR5 receptor antagonists in preclinical to phase II clinical development for treatment of HIV”. Expert Opinion on Investigational Drugs, 2016 VOL. 25, NO. 12, 1377–1392. http://dx.doi.org/10.1080/13543784.2016.1254615 hERG = human ether-a-go-go-related gene DFC

9 C i d a ra ’s P i p e l i n e Ta rg e t s M u l t i p l e U n m e t M e d i c a l N e e d s CLOUDBREAK ANTIVIRAL CLOUDBREAK ONCOLOGY

10 I n f l u e n z a w o r l d w i d e d e a t h r a t e s > 6 5 0 , 0 0 0 p e r y e a r 2 T h e P ro b l e m : A “ U n i v e rs a l ” F l u Va c c i n e D o e s n o t E x i s t Low vaccine effectiveness General population (5-year flu season average) Immunocompromised ~40% 1 ~ 5% 4 Few viable programs in development 2020-2024 Flu season average 3 Co-morbidities at higher risk of hospitalization: Chronic lung disease: 9-fold increase Kidney disease: 5-fold increase Cardiovascular Disease: 12-fold increase 1. https://www.cdc.gov/flu/vaccines-work/past-seasons-estimates.html 2. Estimates of global seasonal influenza-associated respiratory mortality: a modelling study. Lancet. 2018 Mar 31;391(10127):1285-1300. 3. Laboratory-Confirmed Influenza Hospitalizations (cdc.gov) 4. Hughes K, Middleton DB, Nowalk MP, et al. Effectiveness of Influenza Vaccine for Preventing Laboratory-Confirmed Influenza Hospitalizations in Immunocompromised Adults. Clin Infect Dis. 2021;73(11): e4353-e4360. Antigenic drift

11 C D 3 8 8 D e v e l o p m e n t D ata C o n f i r m t h e Ta rg e t P ro d u c t P ro f i l e ( T P P ) Single dose / ̴ 4-6 months Promising Phase 2a data CD388 Neuraminidase inhibitor (NAI) TM Potential for Universal protection Potential to protect high-risk groups Potential for prevention and treatment Scale and cost High Yes Attractive DFCs Yes C D 3 8 8 i s b e i n g d e v e l o p e d f o r p r e - e x p o s u r e p r o p h y l a x i s f o r i n f l u e n z a Study summary at https://clinicaltrials.gov/ct2/show/NCT05285137

12 O p p o r t u n i t y : F i r s t “ U n i v e r s a l ” I n f l u e n z a P r e v e n t a t i v e • Reacquired Global Development and Commercial Rights from Janssen April’24 • Phase 2a results achieved safety, efficacy and PK objectives • Coverage of diverse panels of seasonal and pandemic strains1 • Single SQ or IM dose per flu season • Streamlined, low-cost manufacturing process, low cost of goods (COGs) • High concentration formulations, compatible with SQ or IM dosing • Low immunogenicity • Well-tolerated in Phase 1 and 2a C D 3 8 8 h a s t h e p o t e n t i a l t o b e t h e f i r s t t h e r a p e u t i c t o p r o v i d e s e a s o n - l o n g , u n i v e r s a l i n f l u e n z a p r o t e c t i o n CD388 Neuraminidase inhibitor (NAI) TM Phase 2a clinical proof of concept supports advancement to pivotal studies 1. Based on preclinical data. SQ = Subcutaneous; IM = Intramuscular

13 C o m p re h e n s i v e G l o b a l I P P ro t e c t s C D 3 8 8 E xc l u s i v i t y CD388 Zanamivir Dimer Linker DAR Fc Portfolio Highlights: • Global Portfolio Pending in 31 Jurisdictions • Eight Patent Families Directed to: − CD388 Composition of Matter* − Fc Construct Composition of Matter − Conjugation Methods* − Dosing Regimens • CD388 Composition of Matter Coverage Includes: − Zanamivir Conjugation Point Optionality* − Multiple Covalent Linker Options (length, composition, dimer spacer)* − Wide Drug-Antibody Ratio (DAR) Range* T w o I s s u e d U S C o m p o s i t i o n o f M a t t e r P a t e n t s – U S E x c l u s i v i t y t o S e p t . 2 0 3 9 ( + P T E ) As biologic agents, DFCs are not subject to the IP limitations of the Inflation Reduction Act (IRA) *Included in issued patents PTE = Patent Term Extension

14 C D 3 8 8 I s D i f fe re n t i a t e d F ro m O t h e r I n f l u e n za P ro p hy l a c t i c s Companies in Space Modality Others3 Others3,4 / Others5 DFC (CD388) Stage of Development Spectrum Efficacy in High-Risk Populations Route of Administration Vaccines – strain specific (mRNA, conventional e.g. Fluzone) Vaccines – Universal (mRNA, protein-based) Monoclonal antibodies P2 Universal2 Yes2 SC/IM Approved/P3 Strain specific Low/None3 SC/IM P2/3 Universal Low/None SC/IM Failed/Terminated Influenza A5 Yes IV5 C D 3 8 8 i s t h e m o s t a d v a n c e d s m a l l m o l e c u l e o r p e p t i d e b i o l o g i c c o n j u g a t e i n c l i n i c a l d e v e l o p m e n t 1 1. Based on Clinicaltrials.org. 2. Based on preclinical data. 3. Moderna quadrivalent mRNA vaccine (mRNA 1010) may perform better than conventional vaccines in elderly adults based on Phase 3 topline data https://s29.q4cdn.com/435878511/files/doc_downloads/program_detail/2024/flu-11-02-23.pdf. 4. Gupta and Mohan Journal of Genetic Engineering and Biotechnology (2023) 21:154 https://doi.org/10.1186/s43141-023-00581-y 5. Includes: Celltrion mAb cocktail (CT-P27) (NCT03511066), Medimmune (MEDI8552) (NCT02603952), NIAID/Crucell (CR6261, CR8020) (NCT01992276), Roche (MHAA45498) (NCT02293863), Visterra (Vis410) (NCT03040141 – only tested as treatment). Vir 2482 was IM dosed in a phase 2b prophylaxis study, but failed to meet efficacy endpoints (NCT05567783)

15 C D 3 8 8 : Po t e n t i a l F i rs t “ U n i v e rs a l ” I n f l u e n za P re v e n tat i v e OST = Oseltamivir carboxylate; ZAN = Zanamivir; BXA = Baloxavir acid C D 3 8 8 r e t a i n s p o t e n t a n t i v i r a l a c t i v i t y a c r o s s d i v e r s e s e a s o n a l a n d h i g h p a t h o g e n i c i t y s t r a i n s , i n c l u d i n g H 5 N 1 Cytopathic Effect (CPE) Activity Versus Influenza Strain Panels C D 38 8 O S T ZA N B X A 0.1 1 10 100 1000 10000 E C 5 0 [ n M ] A/H7N9 C D 38 8 O ST ZA N B X A 0.1 1 10 100 1000 10000 E C 5 0 [ n M ] A/H5N1 C D 38 8 O ST ZA N B X A 0.1 1 10 100 1000 10000 E C 5 0 [ n M ] B C D 38 8 O ST ZA N B X A 0.1 1 10 100 1000 10000 E C 5 0 [ n M ] A/H3N2 C D 38 8 O ST ZA N B X A 0.1 1 10 100 1000 10000 E C 5 0 [ n M ] A/H1N1

16 100% survival across broad dose range Protection against body weight loss Po t e n t i a l fo r S i n g l e D o s e , L o n g - A c t i n g P re v e n t i o n i n L e t h a l M o d e l s Exposure selected for clinical development Survival1 Body Weight C D 3 8 8 h a s t h e p o t e n t i a l t o b e t h e f i r s t t h e r a p e u t i c t o p r o v i d e s e a s o n - l o n g , u n i v e r s a l i n f l u e n z a p r o t e c t i o n CD388 protected mice from lethal infection across broad panels of influenza H1N1, H3N2, B/Vic and B/Yam strains at doses ≤ 1 mg/kg 1. Treatment initiated 2 hours post viral challenge. A/Puerto Rico/8/1934(H1N1). Single IM dose.

17 C D 3 8 8 R e t a i n s I n V i v o A c t i v i t y A g a i n s t H i g h l y N A I R e s i s t a n t S t r a i n s Strain Neuraminidase inhibition IC50 (nM) Protective dose (mg/kg) CD388 Zanamivir CD388 Zanamivir B/Laos/0080/2016 H134 (NAI-S) 7.44 2.61 0.3 1 B/Laos/0654/2016 H134N (NAI-R) 4.66 310.8 0.3 10 P r o t e c t i v e d o s e o f C D 3 8 8 d o e s n o t s h i f t i n m i c e i n f e c t e d w i t h m a t c h e d N A I s e n s i t i v e a n d N A I r e s i s t a n t s t r a i n s B/Laos/0654/2016 - H134N1B/Laos/0080/2016 - NAI Sensitive1 1. 5 animals/group treated a single IM dose of CD388 2-hours after viral challenge. Zanamivir dosed IN once daily for 5-days starting 2-hours after infection. Survival monitored for 21 days

18 Ve hi cle Os el ta m ivi r 5 0 m g/ kg CD 38 8 0. 1 m g/ kg CD 38 8 0. 3 m g/ kg CD 38 8 1 m g/ kg CD 38 8 3 m g/ kg Un in fe ct ed 103 104 105 106 107 108 P F U /g *** *** *** *** C D 3 8 8 Re d u c e s V i ra l B u rd e n i n L u n g BLQ Study Details: • Mouse adapted A/Puerto Rico/8/1934 (H1N1) (n=5 mice/arm) • Treatment initiated 2 hours post infection • Oseltamivir dosed twice daily (10x human equivalent dose) • CD388 dosed once • Viral burden assessed four days after lethal challenge U n l i k e o s e l t a m i v i r , C D 3 8 8 d e m o n s t r a t e s r o b u s t , d o s e d e p e n d e n t v i r a l c l e a r a n c e i n l u n g s Viral burden in lung *** P < 0.001 CD388 potently inhibits NAI resistant strains with improved pharmacodynamics

19 C D 3 8 8 P ro p e r t i e s E n a b l e F l ex i b l e D o s i n g O p t i o n s Bioavailability of multiple formulations highlights potential for SC dosing in oncology indications E q u i v a l e n t e f f i c a c y w h e t h e r d o s e d v i a I V , s u b c u t a n e o u s o r i n t r a m u s c u l a r i n j e c t i o n 1 1. Treatment initiated 2 hours post viral challenge. A/Puerto Rico/8/1934(H1N1)

20 C D 3 8 8 N o n c l i n i c a l S u m m a r y D a t a s u p p o r t p o t e n t i a l f o r s i n g l e d o s e “ u n i v e r s a l ” p r e v e n t i o n a n d t r e a t m e n t • Potent in-vitro and in-vivo activity against all tested seasonal and pandemic strains of influenza A and B, including strains resistant to zanamivir and tamiflu (neuraminidase inhibitors) • Equivalent exposure and efficacy via IV, subcutaneous or intramuscular administration • Equivalent efficacy in immune-competent and immune compromised mouse models • Supports potential for single dose of 1.0 mg/kg to provide protection for flu season Efficacy & PK • Well-tolerated at doses up to 500 mg/kg (vs projected 1.0 mg/kg efficacious dose for 100% protection in lethal models) • Anti-drug antibodies directed to the human Fc fragment, not the targeting moiety (TM) • No concerning findings in reproductive or genotoxicity studies Safety

21 O b j e c t i v e s o f Ea r l y C l i n i c a l P ro g ra m s Can CD388 be used for seasonal prophylaxis of influenza?Pharmacokinetics Is CD388 well-tolerated and amenable for prophylactic use?Safety Does CD388 exhibit activity against influenza in the respiratory tract of humans?Efficacy

22 P h a s e 1 a n d P h a s e 2 a C l i n i c a l S t u d i e s A Phase 1, Randomized, Double-Blind, Single-Dose and Repeat Single Dose, Dose-Escalation Study to Determine the Safety, Tolerability, and Pharmacokinetics of CD388 Intramuscular or Subcutaneous Administration in Healthy Subjects (63 subjects) First in human Phase 1 study A Phase 1, Randomized, Double-Blind, Single Ascending Dose Study to Determine the Safety, Tolerability, and Pharmacokinetics of CD388 Subcutaneous Administration in Healthy Japanese Subjects (21 subjects) Japan bridging Phase 1 study A proof-of-concept, randomized, double-blind, placebo-controlled, Phase 2A study to assess the prophylactic antiviral activity against influenza, safety, tolerability, and pharmacokinetics of CD388 via a human viral challenge model (30 subjects) Phase 2a study

23 C D 3 8 8 Wa s We l l - To l e ra t e d fo r U p To 9 0 0 M G Dose FIH JBS HCS Total 50 mg 18 7 2 27 150 mg 18 7 28 53 450 mg 18 7 0 25 900 mg 9 0 0 9 All Doses 63 21 30 114 Number of participants that received one dose of CD388 in Phase 1 and Phase 2a studies (as of Aug 2023) FIH- First in Human study; JBS- Japanese Bridging study; HCS- Human Challenge study Safety Summary • No treatment-emergent SAEs and no discontinuation of study drug or withdrawals due to safety findings • No consistent AE patterns • No hypersensitivity reactions • Most TEAEs Grade 1 (90%), few Grade 2, all resolved • Incidence of TEAE not dose-dependent • Few injection site events (pain, IM route mainly), Grade 1, all resolved spontaneously • No clinically relevant ECG, vital signs or physical exam abnormalities S a f e t y d a t a f r o m F i r s t - i n - H u m a n , J a p a n e s e B r i d g i n g a n d H u m a n C h a l l e n g e s t u d i e s SAEs = Serious Adverse Events; TEAE= Treatment Emergent Adverse Events

24 Endpoint Placebo N=28 CD388 150 mg N=28 P-value qRT-PCR confirmed influenza infection * 14 (50%) 6 (21%) 0.0248 qRT-PCR confirmed symptomatic influenza infection ** 9 (32%) 4 (14%) 0.1023 qRT-PCR confirmed moderately to severe symptomatic influenza infection *** 7 (25%) 3 (11%) 0.1477 Primary endpoint: AUC viral load-time_ qRT-PCR One sided p-value Wilcoxon rank sum test: 0.0390 Mean VL from qRT-PCR Visit/Timepoint Mean – 95% Confidence interval Placebo CD388 150 mg C D 3 8 8 D e m o n st ra t e d Ef f i c a c y i n P h a s e 2 a *RT-PCR-confirmed influenza infection: 2 quantifiable (≥ lower limit of quantification [LLOQ]) qRT-PCR measurements (reported on 2 or more independent samples over 2 days), from Day 1 (pm) up to Day 8 (am). **RT-PCR-confirmed symptomatic influenza infection: RT-PCR-confirmed influenza infection (2 quantifiable [≥LLOQ] qRT-PCR measurements [reported on 2 or more independent samples over 2 days]), from Day 1 (pm) up to Day 8 (am), AND symptoms ≥2 at a single time point. ***RT-PCR-confirmed moderate to severe symptomatic influenza infection: RT-PCR confirmed influenza infection (2 quantifiable [≥LLOQ] qRT-PCR measurements [reported on 2 or more independent samples over 2 days]), from Day 1 (pm) up to Day 8 (am), AND any symptoms of grade ≥2 at a single time point. M ea n ( +/ - C I 9 5 % ) - V L fr o m q R T -P C R ( lo g1 0 c o p ie s/ m L)

25 Mean – 95% Confidence interval *, * = mean. Placebo median = 0.50; CD388 150 mg median = 0.50 Mean VL from Viral Culture Peak Viral Load from Viral Culture Placebo CD388 150mg TreatmentVisit/Timepoint Placebo CD388 150 mg V i ra l C u l t u re D ata C o n f i r m e d Ef f i c a c y S e e n i n Ea r l y A n a l ys e s M e an ( +/ - C I 9 5 % ) - V L fr o m V ir al C u lt u re ( lo g1 0 T C ID 5 0 /m L) P e ak V ir al L o ad f ro m V ir al C u lt u re ( lo g1 0 TC ID 5 0 /m L)

26 P h a s e 2 b C D 3 8 8 I n f l u e n za P re v e n t i o n S t u d y P l a n n e d i n Fa l l 2 0 2 4 P h a s e 2 b D o u b l e - B l i n d R C T f o r t h e E f f i c a c y / S a f e t y o f C D 3 8 8 v s P l a c e b o i n t h e P r e v e n t i o n o f I n f l u e n z a • Study Design: Blinded, randomized, controlled trial with single doses of CD388 or placebo administered at the beginning of the influenza season with subjects followed for the entire influenza season to monitor for breakthrough cases of influenza • Primary Endpoint: To compare the rates of laboratory-confirmed clinical influenza between different single doses of CD388 and placebo over an influenza season • Study Population: Generally healthy adults (patients at high-risk of complications from influenza excluded) • Seasonal influenza vaccines also excluded • Study Size: Target of 4000 subjects with possible increase to a maximum of 6000 subjects (depending on the rate of influenza infection) with three CD888 dose groups and 1 placebo group randomized in a 1:1:1:1 ratio Planned Phase 3 study in subjects at high risk of developing complications from influenza RCT = Randomized Clinical Trial

27 2024 2025 2026 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 C D 3 8 8 P h a s e 2 b E s t i m at e d D e v e l o p m e n t T i m e l i n e CD388 Phase 2B Study (n ~4,000) 2 Northern Hemisphere Flu Season Southern Hemisphere Flu Season* 1 Actual timelines may differ materially due to severity of flu season, rate of patient enrollment etc. 1 Topline Data if NH only 2 Topline Data if NH & SH * If needed

28 C D 3 8 8 : A Po t e n t i a l M u l t i - B i l l i o n D o l l a r M a r ke t O p p o r t u n i t y 1 Source: Influenza Global Flu market till 2032 (2023-2032 CAGR 11.07%). https://www.globenewswire.com/en/news-release/2024/03/05/2840453/0/en/Global-Influenza-Vaccine-Market-to-Attain-Valuation-of-USD-22-71-Billion-By-2032-Astute-Analytica.html 2. https://www.nyc.gov/site/doh/providers/health-topics/influenza-high-risk-groups.page; CAGR = Compounded Annual Growth Rate; HIV = human immunodeficiency virus. $8.78B(1) $22.7B(1) 2023 2032 • Potential for universal protection • Potential to protect all high-risk groups • Potential for prevention and treatment​ • Attractive scale and cost CD388 Target Product Profile & Positioning • Growth due to rise of more effective vaccines • Expansion due to: – Next generation premium flu vaccines – Better prophylactic agents – New therapeutic modalities with improved efficacies Market Growth and Expansion ExpectedGlobal Influenza Vaccine Market % Market Share of Influenza High-Risk Groups 2 (18 and older) • Adults 18 and older • Immunocompromised or weakened immune systems (e.g., HIV, cancer or on immunosuppressive drugs) • People with certain health conditions {diabetes, lung disease, asthma, heart disease, sickle cell anemia, kidney or liver disease, metabolic disorders, and disorders than may cause breathing problems (e.g., muscle, nerve disorders)} • People who are overweight - Body Mass Index (BMI) 40 or over • People living in nursing homes and other care facilities • Those who are in close contact with people at high risk of complications (e.g., healthcare workers) % Market Share of Traditional and Premium Vaccine Market % Market Share of Worldwide Opportunity

29 Estimated Peak Sales 2 Multi-billion dollar potential $5.6bn $5.2bn $2.9bn $3.9bn $5.9bn1 Modality DFC mRNA Vaccine mAb mRNA Vaccine Quadrivalent mod RNA Vaccine (mRNA vaccine) Quadrivalent Vaccine (egg and Cell based) Current Status Phase 2 Phase 2/3 Terminated Phase 2 Phase 3 Commercial Broker / Source N/A William Blair 7/24/2023 Needham 5/5/2023 Goldman Sachs 12/11/2023 HSBC 7/2023 CDC B e n c h m a r k s o f E s t i m a t e d P e a k S a l e s f o r S e l e c t e d P ro p hy l a c t i c F l u P ro g ra m s 1. FY 2022 total revenue estimates based on CDC and individual Company data; includes Flumist, Fluarix, FluLaval, Fluzone, Fluzone HD, Flubloc, Afluria, Flucelvax & Fluad. 2. Estimated Peak Sales at 100% POS. Patient population and addressable market for each program may not be similar. / / / Traditional Vaccines 1

30 C i d a ra ’s P i p e l i n e Ta rg e t s M u l t i p l e U n met M e d i ca l N e e d s CLOUDBREAK ANTIVIRAL CLOUDBREAK ONCOLOGY

31 C l o u d b re a k O n c o l o g y D F C P ro g ra m s CD73: CBO421 Development Candidate • Differentiated from existing SM and mAb CD73 inhibitors • Complete responders in combination with PD-1 inhibitors • Excellent safety and COGS PD-1/CD73 Discovery Program • Unique dual inhibitor of CD73 and PD-1 • Compelling preclinical data • Potential for more efficient clinical development CCR5 Discovery Program • Overcomes limitations of prior approaches • Proof of concept data against “undruggable” target • Potential for improved safety over SM antagonists mAbs = Monoclonal Antibodies; SM= Small Molecule

32 C l o u d b re a k O n c o l o g y D F C P ro g ra m s CD73: CBO421 Development Candidate • Differentiated from existing SM and mAb CD73 inhibitors • Complete responders in combination with PD-1 inhibitors • Excellent safety and COGS PD-1/CD73 Discovery Program • Unique dual inhibitor of CD73 and PD-1 • Compelling preclinical data • Potential for more efficient clinical development CCR5 Discovery Program • Overcomes limitations of prior approaches • Proof of concept data against “undruggable” target • Potential for improved safety over SM antagonists

33 Rationale for CD73 • Adenosine creates an immune suppressive Tumor Microenvironment (TME) by reprogramming multiple immune cell classes • Dying tumor cells release ATP into the TME which subsequently gets converted into adenosine by CD73 • CD73 inhibitors are an ideal partner for chemotherapy Mast Cells M2 Macrophage NK Cells MDSCs Dendritic Cells Tregs Effector T Cells TME remodeling and angiogenesis Antigen presentation Adenosine Tumor Immunosuppression A d e n o s i n e i s a n I m p o r ta n t M e d i a t o r o f Tu m o r I m m u n e Eva s i o n Image reprinted from Harvey JB, Phan LH, Villarreal OE and Bowser JL (2020) CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers. Front. Immunol. 11:508.

34 C D 7 3 C l i n i c a l D ata To D at e H a s B e e n D i s a p p o i n t i n g Therapy Drug Class Safety Profile Single agent activity Combination Efficacy Oleclumab (AstraZeneca) mAb Benign None1 With anti-PD-L1 in stage III NSCLC2: • ORR 30% (vs. 17.9%) • No additional CR’s achieved beyond PD-L1 single agent activity NZV930 (Novartis) mAb Benign None; monotherapy trial halted due to poor efficacy Studies in progress in combo with other immune therapies3 ORIC-533 (Oric) SM Benign Study in progress4 No studies found • No Approved Drugs • Significant potential to improve CD73 inhibitors 1. Kondo S et al. Int. J. Clin. Oncol., 27 (2022), pp. 1795-1804 2. Herbst R et al. J Clin Oncol. (2022) Oct 10;40(29). NSCLC = Non-Small Cell Lung Cancer. 3. https://doi.org/10.1158/1538-7445.AM2022-CT503 4. https://doi.org/10.1182/blood-2023-173730; I s C D 7 3 a v a l i d ta r g e t ? Cidara’s next generation inhibitor combines robust catalytic inhibition of soluble and cell anchored CD73 with receptor internalization for potential enhanced performance in the clinic mAbs = Monoclonal Antibodies; SM= Small Molecule

35 Ph2 COAST trial in stage III NSCLC R e c e n t P h a s e 1 b D a t a S u p p o r t s C D 7 3 a s a Va l i d Ta r g e t : I m p r o v e d O v e r a l l S u r v i v a l C o m b i n i n g C D 7 3 I n h i b i t o r W i t h C h e m o t h e r a p y 1. Wainberg et al. GI ASCO 2024 poster https ://doi.org/10.1200/JCO.2024.42.3_suppl.665 D e s p i t e s e l e c t i o n o f a n i n f e r i o r s t a n d a r d o f c a r e c h e m o t h e r a p y p a r t n e r i n t h e A R C - 8 s t u d y

36 C B O 4 2 1 E m e rg i n g a s a D i f fe re n t i a t e d C D 7 3 T h e ra p y CBO421 CD73 ADO X AMP • Differentiated from existing SM and mAb CD73 inhibitors • Highly stable with excellent pharmaceutical properties • ~65 kDa (vs > 150 kDa for mAbs) – better tumor penetration • Inhibits both membrane bound and soluble CD73, downregulates CD73 via internalization • Ideal combination partner agent with PD-1/L1 axis inhibitors and chemotherapy • Robust manufacturing process

37 C B O 4 2 1 E x h i b i t s D i f fe re n t i a t e d P re c l i n i c a l Pe r fo r m a n c e Differentiated from Existing Adenosine Pathway Inhibitors PBMC rescue assay (ATP) vs clinical stage adenosine pathway inhibitors Potent Anti-Tumor Activity as Monotherapy MC38 – murine colorectal carcinoma AB680 CD73 inhibitor Oleclumab CD73 inhibitor biosimilar IPH5201 CD39 inhibitor biosimilar AB928 A2AR inhibitor CPI-444 A2AR inhibitor Test article Target/Class EC50 [nM] CD4+CD25+ CD8+CD25+ CBO421 CD73/DFC 13 51 AB680* CD73/small molecule 39 73 Oleclumab CD73/mAb >1,000 >1,000 IPH5201 CD39/mAb >1,000 >1,000 AB928 A2AR/small molecule >1,000 >1,000 CPI-444 >1,000 >1,000 Tumor Volume (MC38) (10 mg/kg dose, 2x/wk)Tumor volume (mm³) Days post tumor cell injection 0 300 600 900 1200 1500 10 15 20 P=0.0052 Vehicle CBO421

38 Tu m o r C o n t ro l : C B O 4 2 1 E x h i b i t s S u p e r i o r Tu m o r Pe n e t rat i o n v s . m A b s CD421 Oleclumab 0 50 100 150 200 250 300 0.0 0.1 0.2 0.3 0.4 CBO421 Relative Fluorescence Intensity Edge Center MDA-MB-231* Spheroids Study conducted by PhenoVista Biosciences MDA-MB-231 cell line was isolated at MD Anderson, is ER, PR, and E-cadherin negative, and expresses mutated p53. It is commonly used to represent a model of TNBC.

39 MC38 – murine colorectal carcinoma C B O 4 2 1 E n h a n c e s A n t i - t u m o r A c t i v i t y O f P D - 1 I n h i b i t o rs Study Arm % Responders2 Vehicle 0 CBO421 27 Anti-PD-11 47 CBO421 + Anti-PD-11 60 1. *RMP1-14 2. Defined as mice that demonstrate cessation of tumor growth or reduction in tumor volume across two or more timepoints. C B O 4 2 1 + A n t i - P D - 1 c o m b i n a t i o n i m p r o v e s r e s p o n s e r a t e s v e r s u s m o n o t h e r a p y

40 Survival (Day 62) Compounds dosed 2x weekly for 22 days Survivor rechallenge EMT6 tumor cells C B O 4 2 1 E l i c i t s C o m p l e t e Re s p o n s e s w i t h P D - 1 I n h i b i t o rs D+62 (re-challenge) Last dose (D+22) 40-day washout period Study start (D+0) D+73 EMT6 – murine mammary carcinoma 40% of mice in combination arm demonstrated complete responses All complete responses persisted *RMP1-14 C B O 4 2 1 + A n t i - P D - 1 c o m b i n a t i o n i m p r o v e s s u r v i v a l a n d i n d u c e s i m m u n o l o g i c a l m e m o r y

41 CD73 expression increases in response to chemotherapy, creating a pro-tumorigenic environment1 • Small molecule CD73 inhibitors have no effect on CD73 levels, and can be overwhelmed by increasing ADO levels induced by chemotherapy • mAb CD73 inhibitors are limited by inferior catalytic inhibition but some reduce CD73 levels via receptor internalization • CBO421 uniquely counteracts tumor adaptations to chemotherapy by combining potent catalytic inhibition and receptor internalization C h e m o t h e ra p y C re at e s a Fe e d b a c k L o o p T h at C a n O v e r w h e l m C u r re n t C D 7 3 I n h i b i t o r C l a s s e s AMP ADO (adenosine) Tumors release soluble CD73 CD73 CD73 levels ADO Soluble CD73 Metastasis Suppression/repolarization of immune cells 1. Bach, N. et al. Int. J. Mol. Sci. 2023, 24, 11759. https://doi.org/10.3390/ijms241411759 C D 7 3 i n h i b i t o r s p o t e n t i a t e c h e m o , b u t e f f e c t s c a n b e a t t e n u a t e d b y t u m o r a d a p t a t i o n s

42 ≥ 1 nM concentrations, CBO421 removes detectable cell anchored CD73 from the cancer cell surface L o w C B O 4 2 1 C o n c e n t rat i o n s R a p i d l y Re d u c e C D 7 3 L e v e l s o n C D 7 3 + T N B C C e l l s ( M DA - M B - 2 3 1 ) * 1 nMUntreated 0.001 nM 0.01 nM 0.1 nM *MDA-MB-231 cell line is ER, PR, and E-cadherin negative and expresses mutated p53 and commonly used to represent TNBC.

43 Test article Target/Class Maximum % internalization EC50 [nM] CBO421 CD73/DFC 81 0.07 AB680* CD73/small molecule 0* NA Oleclumab# CD73/mAb 38 0.27 C o m b i n at i o n o f Re c e p t o r I n t e r n a l i za t i o n a n d Po t e n t C ata l y t i c I n h i b i t i o n Po s i t i o n s C B O 4 2 1 a s a n I d e a l C h e m o t h e ra p y Pa r t n e r CD73 Internalization on MDA-MB-231 tumor cells by flow cytometry (4 hours post incubation) °MDA-MB-231 cell line was isolated at MD Anderson, is ER, PR, and E-cadherin negative, and expresses mutated p53. It is commonly used to represent a model of TNBC. *AB680 – Arcus Biosciences CD73 inhibitor, internalization data not shown #Oleclumab – Astra Zeneca biosimilar CD73 inhibitor CBO421 combines potent CD73 inhibition and CD73 downregulation, distinguishing it from small molecule and mAb CD73 inhibitors in clinical trials

44 Lacks ER, PR, and HER21: no targeted or hormonal therapies available C B O 4 2 1 D e v e l o p m e n t f o r H i g h U n m e t N e e d T N B C P o p u l a t i o n s L e v e ra g e s Po t e n t i a l B e n e f i t o f C D 7 3 / C h e m o C o m b i n a t i o n T h e ra p y Triple Negative Breast Cancer (TNBC): An opportunity for CBO421 to dramatically change the course of disease Young patients: majority diagnosed before age 502 10% present with metastatic disease; another 30-50% develop metastatic disease after initial treatment3 TNBC expresses high levels of soluble CD73 with correlation to poor prognosis and resistance to chemotherapy8 Standard of care is chemotherapy backbone which provides median survival of 12-15m3,4 • For PD-L1+ (CPS ≥ 10): SOC is pembrolizumab + chemotherapy but only 30% are eligible5 • For BRCA-mutation+, SOC is PARP-I or chemotherapy but only 10-15% are eligible6 • High unmet need: approximately 50% of patients are neither CPS10+ nor BRCA+ • Chemotherapy remains backbone of every effective treatment for TNBC7 1. Wolff et al. 138, 241–256. 10.5858/arpa.2013-0953. 2. McGuire et al. Cancers 7, 908–929. doi:10.3390/cancers7020815 3. Dent et al. Clin Cancer Res. 2007; 13: 4429-4434 4. Kim et al. Lancet Oncol. 2017 18, 1360–1372 5. Flavia et al. Cancers (Basel). 2023 Jun; 15(11): 2933 6. Gonzales-Angulo et al. Clin Cancer Res. 2011;17(5):1082–1089 7. Zeichner et al. Breast Cancer (Auckl). 2016; 10: 25-36 8. Loi et al. Proc. Natl. Acad. Sci. U.S.A. 2013: 110, 11091–11096 ER = Estrogen Receptor; PR= Progesterone Receptor

45 P l a n n e d F i rs t - i n - H u m a n C l i n i ca l Tr i a l s fo r C B O 4 2 1 2024 2025 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 IND Submission Phase 1 Study in Solid Tumors (including TNBC) GLP Toxicity Study (in-life complete)* Pre-clinical Clinical Actual timelines may differ materially due to timing of site initiation, patient enrollment, etc. Regulatory *Based on current results, NOAEL = 500 mg/kg/week (Interim results expected: Biomarker and PK/PD ​)

46 C l o u d b re a k C D 7 3 / P D - 1 B i s p e c i f i c D F C s CD73: CBO421 Development Candidate • Differentiated from existing SM and mAb CD73 inhibitors • Complete responders in combination with PD-1 inhibitors • Excellent safety and COGS PD-1/CD73 Discovery Program • Unique dual inhibitor of CD73 and PD-1 • Compelling preclinical data • Potential for efficient clinical development CCR5 Discovery Program • Overcomes limitations of prior approaches • Proof of concept data against “undruggable” target • Potential for improved safety over SM antagonists

47 Po t e n t i a l F i rs t - i n - C l a s s P D - 1 / C D 7 3 I n h i b i t o r D i s a b l e s Tw o M a j o r Tu m o r I m m u n e E s c a p e M e c h a n i s m s i n a S i n g l e M o l e c u l e CD73 inhibitor Killer T-cell PD-1 CD73 CD73 PD-1 inhibitor PD-L1 Cidara’s first multispecific DFC (PD-1/CD73) is a unique dual inhibitor Engineered to improve efficacy by disabling a key resistance mechanism to PD-1 inhibitors

48 CTP-PD-1 PD-1/CD73 DFC CD73 DFC P D - 1 / C D 7 3 D F C Po t e n t l y I n h i b i t s B o t h P D - 1 a n d C D 7 3 Re c e p t o rs CD73 inhibitor PD-1 Binding (IC50, nM) – 0.056 T-cell reactivation (EC50, nM) – 12 PD-1 Binding (IC50, nM) – 0.064 T-cell reactivation (EC50, nM) – 9 PD-1 inhibitor

49 P D - 1 / C D 7 3 D F C D e m o n st ra t e s S u p e r i o r Tu m o r G ro w t h I n h i b i t i o n v s M o n o t h e ra p i e s i n H u m a n i ze d Tu m o r M o d e l s Tumor Volume (MC38, hPD-L1), day 22 hPD-1/hPD-L1 C57BL/6 mice – 2X weekly dosing Tumor Volume (MC38, hPD-L1), day 22 hPD-1/hPD-L1 C57BL/6 mice – 2X weekly dosing Veh ic le (P B S) P em br ol iz um ab (1 0 m g/ kg ) C B O 42 1 (1 0 m g/ kg ) P D -1 /C D 73 D FC (3 m g/ kg ) 0 500 1000 1500 2000 Tumor Volume (MC38, hPD-L1), day 22 hPD-1/hPD-L1 C57BL/6 mice 2X weekly dosing T u m o r v o lu m e ( m m 3 ) p = 0.007 p = 0.03

50 Dendritic cells (DCs) express CD73 and PD-L1/L2 P D - 1 / C D 7 3 I m p ro v e s Re l e a s e o f I m m u n e S u p p re s s i o n Do no r 1 P BM Cs Do no r 1 P BM Cs + D on or 2 D Cs 30 0µ M A M P CB O4 21 PD -1 D FC PD -1 /C D7 3 DF C 0 1000 2000 3000 IL -2 ( p g/ m L) ns * ** Do no r 1 P BM Cs Do no r 1 P BM Cs + D on or 2 D Cs 30 0µ M A M P CB O4 21 PD -1 D FC PD -1 /C D7 3 DF C 0 5000 10000 15000 20000 IF N -g ( p g /m L ) ns * ** P D - 1 / C D 7 3 D F C r e l e a s e s i m m u n e s u p p r e s s i o n m e d i a t e d b y a d e n o s i n e a n d P D - 1 / L 1 i n 1 - w a y m i x e d l y m p h o c y t e r e a c t i o n a s s a y ** P < 0.01 * P < 0.05

51 * ns * Tumor Volume (MC38, hPD-L1) hPD-1/hPD-L1 C57BL/6 mice – 2X weekly dosing Tumor Volume (MC38, hPD-L1) hPD-1/hPD-L1 C57BL/6 mice – 2X weekly dosing P D - 1 / C D 7 3 D F C D e m o n st ra t e s Ro b u st Tu m o r G ro w t h I n h i b i t i o n * ** ** P D - 1 / C D 7 3 D F C r e t a i n s s t a t i s t i c a l l y s i g n i f i c a n t t u m o r g r o w t h c o n t r o l a t l o w e r d o s e s ** P < 0.01 * P < 0.05 *PD-1 is the proprietary PD-1 inhibitor used in the multispecific PD-1/CD73 DFC

52 C i d a ra ’s P D - 1 / C D 7 3 D F C i s D i f fe re n t i a t e d Attribute PD-1/CD73 DFC AK131 Potential for differentiation with PD-1/CD73 DFC Size < 125 kDa > 200 kDa Superior tumor penetration, better potential for high concentration formulations Inhibition of CD73 catalytic activity Full Partial* Superior inhibition of CD73 Retention of component monotherapy activity in multispecific format Full Partial* Efficacy at lower doses Cidara PD-1/CD73 DFC – Preclinical Akeso bispecific mAb (AK131) – Phase 1a opened (Dec 2023) *Based on data presented in: Cancer Res (2022) 82 (12_Supplement): 5526. https://doi.org/10.1158/1538-7445.AM2022-5526 C i d a r a ’s D F C a n d A k e s o ’s b i s p e c i f i c m A b a p p e a r t o b e t h e m o s t a d v a n c e d P D - 1 / C D 7 3 m u l t i s p e c i f i c a g e n t s i n d e v e l o p m e n t

53 Attribute ADC Bispecific mAb DFC Advantage of DFC Example Sacituzumab Govitecan Enfortumab Vedotin PD-1/LAG3 PD-1-CTLA4 PD-1/CD73 PD-1/CD73 Size >150kDa > 200 kDa < 125 kDa Smaller size allows enhanced tumor penetration Cytotoxic component Yes No No No chemotherapy component allows enhanced safety profile Linker Cleavable Stable Stable MOA not restricted to internalization only Not limited by lower therapeutic efficiency in case of inefficient intracellular trafficking P D - 1 / C D 7 3 D FC O f fe rs A d va nta g e s O ve r B o t h C y t o t ox i c A D C s a n d B i s p e c i f i c m A b s * DFCs allow for use of combined targeting modalities (peptides and small molecules) offering unique combinations, smaller size, tunable multivalent binding and enhanced safety *Based on data from Shim et al. Biomolecules. 2020 Feb 26;10(3):360

54 P D - 1 / C D 7 3 C l i n i c a l D e v e l o p m e n t S t ra t e g y – A F i rs t i n C l a s s O p p o r t u n i t y • Potential first-in-class, novel molecule: clinical trials historically enroll faster • Single infusion of multi-specific DFC vs. sequential infusions of 2 separate therapeutics: limits infusion chair time; patient-friendly; oncology office friendly* • Opportunity to be evaluated in earlier lines of development where PD-1/L1 agents are established SOC • PD-1/CD73 clinical development may be expedited due to having already shown contribution of components with CBO421 • Development candidate selection anticipated mid-2024 *Sugalski JM, Kubal T, Mulkerin DL, et al: National Comprehensive Cancer Network Infusion Efficiency Workgroup study: Optimizing patient flow in infusion centers. J Oncol Pract 15:e458-e466, 2019

55 C l o u d b re a k C C R 5 D F C P ro g ra m CD73: CBO421 Development Candidate • Differentiated from existing SM and mAb CD73 inhibitors • Complete responders in combination with PD-1 inhibitors • Excellent safety and COGS PD-1/CD73 Discovery Program • Unique dual inhibitor of CD73 and PD-1 • Compelling preclinical data • Potential for more efficient clinical development CCR5 Discovery Program • Overcomes limitations of prior approaches • Proof of concept data against “undruggable” target • Potential for improved safety over SM antagonists

56 CCR5 signaling promotes immune cell migration to tumor, where they are “educated” in the TME to become immunosuppressive (e.g. TREGS, tumor-associated macrophages (M2-TAMs) Tumor cells “hijack” CCR5 signaling to induce tumor growth, angiogenesis, chemotherapy resistance CCR5-DFC CCR5 Antagonist X CCR5 CCL3/5 CCR5 CCL5/CCR5 is an important driver of tumor growth, immune evasion and metastasis in several difficult to treat cancers* • Breast • Pancreatic • Ovarian • Prostate *Int. J. Mol. Sci. 2022 https://doi.org/10.3390/ijms232214159 C C R 5 : C o m p e l l i n g Ta rg e t T h at D r i ve s P ro g re s s i o n o f H a rd - t o - Tre at C a n c e rs

57 C C R 5 i s a C o m p e l l i n g O n c o l o g y Ta rg e t D e v e l o p m e n t c a n d i d a t e n o m i n a t i o n a n t i c i p a t e d i n m i d - 2 0 2 4 Acts as a “GPS” system that promotes metastatic disease and migration of immune suppressive cells to tumor1,2 • CCR5+ Circulating Tumor Cells (CTCs) and Cancer Associated Macrophage Like cells (CAMLs) promote metastatic disease – good efficacy biomarker • Promotes Treg migration to tumor and macrophage repolarization to promote immune evasion CCR5 CCR5 signaling upregulates DNA repair, angiogenesis in tumors3 CCR5 antagonists could significantly augment chemotherapy and checkpoint blockade therapy4 • CCR5 signaling reduces the effectiveness of chemotherapy • Chemotherapy upregulates CCR5 expression • TNBC, ovarian, prostate and colon cancer 1. Hamid, R. et al. Cells 2023, 12, 2237. https://doi.org/10.3390/cells12182237 2. Raghavakaimal et al. Breast Cancer Research (2022) 24:35 https://doi.org/10.1186/s13058-022-01528-w 3. Jiao et al. Breast Cancer Research (2021) 23:11 https://doi.org/10.1186/s13058-021-01391-1 4. EXPERT OPINION ON THERAPEUTIC TARGETS 2021, VOL. 25, NO. 4, 311–327 https://doi.org/10.1080/14728222.2021.1902505

58 • Enhanced safety profile and compatibility with chemotherapy vs small molecule antagonists • Potential as a combination agent with SOC chemotherapy in TNBC • Potential for development of first in class multispecific therapies • Potential to develop for long-acting HIV retroviral therapy (with partner) Tw o C o m p e t i t o r C C R 5 P ro g ra m s w i t h Kn o w n L i a b i l i t i e s 1. Journal of Clinical Oncology Volume 40, Number 16_suppl https://doi.org/10.1200/JCO.2022.40.16_suppl.e130 2. https://www.cytodyn.com/newsroom/press-releases/detail/618/cytodyn-announces-fda-has-lifted-clinical-hold 3. https://doi.org/10.1016/j.ejca.2022.03.017 4. Drug Metabolism and Disposition May 2019, 47 (5) 493-503; DOI: https://doi.org/10.1124/dmd.118.085241 Anti-CCR5 Drug Class Clinical Data Notes Leronlimab (CytoDyn) mAb Pooled analysis 3 studies in combo with chemotherapy TNBC (n=28): mOS 12+ months1 2019: Fast Track Designation for TNBC 2022: FDA clinical hold due to CMC and data quality concerns – lifted on March 1, 20242 Maraviroc (Pfizer) Small Molecule PICASSO-1 ph1b (n=22) in combo with pembrolizumab mCRC: modest efficacy; G3/G4 AEs noted3 Limited by off-target toxicity and DDI potential4 No further development planned in oncology CCR5 monotherapy and combination DFCs

59 First CCR5 targeting therapy designed for oncology V o lu m e ( m m 3 ) WT mice CCL5 KO mice C C R 5 D F C I n d u c e s Tu m o r Re d u c t i o n C o m m e n s u rat e W i t h a C C L 5 KO M o d e l i n C o l o re c ta l C a rc i n o m a p=0.0089 20 MPK 2X/week 1. Zhang et al. Cell Death and Disease (2018) 9:766 DOI 10.1038/s41419-018-0796-2 CCR5 DFC treatment potently inhibits tumor growth MC38 tumors are unable to proliferate in CCL5 KO mice (MC38 = murine colorectal carcinoma)

60 C l o u d b re a k O n c o l o g y D F C P ro g ra m s CD73: CBO421 Development Candidate • Differentiated from existing SM and mAb CD73 inhibitors • Complete responders in combination with PD-1 inhibitors • Excellent safety and COGS PD-1/CD73 Discovery Program • Unique dual inhibitor of CD73 and PD-1 • Compelling preclinical data • Potential for more efficient clinical development CCR5 Discovery Program • Overcomes limitations of prior approaches • Proof of concept data against “undruggable” target • Potential for improved safety over SM antagonists

61 On April 24, 2024, the Company raised an additional $240 million in gross proceeds in a private placement led by RA Capital Management with significant participation by Bain Capital Life Sciences as well as BVF Partners and Canaan Partners. Important Information December 31, 20231 Cash and Cash Equivalents $35.8M Common Stock Outstanding 90,601,999 Common Equivalent Shares Outstanding2 111,646,719 F i n a n c i a l O v e r v i e w 1. Information listed here is as of December 31, 2023 (as disclosed in our Form 10-K). 2. Includes (i) 90,601,999 shares of common stock and (ii) 21,044,720 shares of common stock issuable upon the conversion of Series X Convertible Preferred stock, both as of December 31, 2023. Each share of Series X Convertible Preferred is convertible into 10 shares of common stock. 3. Amounts reflect a rolling two-quarter period ending on the date noted. Amounts shown are historical and may not be indicative of future results. Summary Consolidated Cash Flow Information Rolling two-quarter period ended December 31, 20233 Operating Cash Burn $(31.9)M Mundipharma Reimbursements $0.4M Janssen Reimbursements & Milestones $15.4M Melinta Milestones & Sales Receipts $1.5M Net Cash Provided by Operations, Investing & Financing (excluding ATM Proceeds) $0.6M ATM Proceeds Less Offering Costs $0.0M Net Cash Decrease $(14.6)M

62 C a p i ta l S t r u c t u re a n d S h a re I n fo r m at i o n All shares in millions 12/31/23 1 (as filed 10-K) 4/24/24 Split -Adjusted (1:20)5 4/24/24 PIPE Financing (Split Adjusted 1:20)5 4/24/24 Pro-forma PIPE Financing & Reverse Split (1:20)5 Common Shares Outstanding 90,601,999 4,530,100 4,530,100 Series X Convertible Preferred stock (as converted) 2 21,044,720 1,052,236 1,052,236 Common stock options, RSUs and PRSUs issued and outstanding 12,764,068 638,203 638,203 Fully Diluted Common Shares Outstanding 124,410,787 6,220,539 6,220,539 240,000 shares of Series A Convertible Voting Preferred Stock (as converted) 3 16,901,408 16,901,408 Pro-forma Fully Diluted Common Shares Outstanding 23,121,9486 Average VWAP Post Reverse Spilt 4/24/24 – Current4 $13.73 Implied Pro-forma Fully Diluted Equity Value / Market Cap $317.5 million Cash and Cash Equivalents $35.8 million $240.0 million $275.8 million7 Debt - - 1. Information listed here is as of December 31, 2023 (as disclosed in our Form 10-K). 2. 21,044,720 shares of common stock issuable upon the conversion of Series X Convertible Preferred stock, both as of December 31, 2023. Each share of Series X Convertible Preferred is convertible into 10 shares of common stock. 3. 240,000 shares of Series A Convertible Voting Preferred Stock, par value $0.0001 per share (the "Series A Preferred Stock”). Each share of Series A Preferred Stock is, subject to stockholder approval and certain beneficial ownership conversion limitations, automatically convertible into shares of common stock, par value $0.0001 per share, at a conversion price of $14.20 per share, rounded down to the nearest whole share. 4. As of 4/29/24. 5. Reverse Split-adjusted numbers are approximate based on a ratio of 1:20. 6. Subject to stockholder approval of an increase in authorized common stock. 7. Pro-forma as of 12/31/23 and PIPE financing on 4/24/24.

63 Thank You May 2024 NASDAQ: CDTX