Slides
Page 1
August 2026 Company Overview NASDAQ : JBIO Jade BIOSCIENCES
Page 2
Disclaimers F OR WA R D L OO K IN G S T A TE ME N TS Certain statements contained in or made orally during this presentation,other than purely historical information, may constitute “forward-looking statements” within the meaning of the federal securities laws, includingfor purposes of the “safe harbor” provisions under the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, but are not limited to, express or implied statements relating to Jade’sexpectations, hopes, beliefs, intentions or strategies regarding the future of its pipeline and business including, without limitation: Jade's cash runway; Jade’s ability to achieve the expected benefits or opportunitieswith respect to JADE101, JADE201 and JADE301,includingtheir best-in-class and best-in-disease potential;the expected timelines forthe availability ofinterim data from the Phase2 clinical trial of JADE101 and the Phase 1 clinical trials of JADE201 and JADE301;the expected enrollment of the Phase 2 clinical trial of JADE101; Jade’s plans to conduct a Phase 3 clinical trial of JADE101, the design and timing thereof and Jade’s expectations that such trial will serve as a registrational study;Jade’s proposed dosing strategy and its expected optimization of clinical activity and convenience; projected or simulated pharmacodynamic outcomes, including steady-state IgA reductions;the potential for the anti-APRILclass to become the foundational therapy for IgAN; the potential for JADE101 healthy volunteer data to be predictive of clinical activity; the potential of Jade's product candidates toenable clinical remission and their potential therapeutic uses, market opportunities, efficacy,durability,safety profiles, and dosing. The words “opportunity,” “potential,” “milestones,” “pipeline,” “can,” “goal,” “strategy,” “target,” “anticipate,” “achieve,” “believe,” “contemplate,” “continue,” “could,” “estimate,” “expect,” “intends,” “may,” “plan,” “possible,” “project,” “should,” “will,” “would” and similar expressions (including the negatives of these terms or variations of them) may identify forward-looking statements, but the absence of these words does not mean that a statement is not forward-looking. These forward-looking statements are based on current expectations and beliefs concerning future developments and their potential effects. There can be no assurance that future developments affecting Jade will be those that have beenanticipated. These forward-looking statements involvea number ofrisks, uncertainties (some of which are beyond Jade’s control) or other assumptions that may cause actual results or performance to be materially different from those expressed or implied by these forward-looking statements. These risks and uncertainties include, but are not limited to:interim results of a clinical trial are not necessarily indicative of final results and one or more of the outcomes may materially change following more comprehensive reviews of the data, as follow-up on the outcome of any particular participant continues and as more participant or final data becomes available;modeledand predicteddata for JADE101may not be realized in actualclinicalstudies andmay notaccuratelyrepresentperformance of third partyagents;the ongoing and planned clinical trials of JADE101 and any other clinical trials may be delayed or may not demonstrate desirable efficacyor predicted performance; Jade’s plannedJADE101Phase 3 clinicaltrial may be delayed based on FDA feedback orrequirements, as the FDA retains broad discretion to require additional clinical data for any product candidateprior to the conduct of a Phase 3 clinical trialor submission forregulatoryapproval;even if such Phase 3 trial is successful,it may not support regulatory approval;adverse events and safety signals may occur; Jade may experience unanticipated costs, difficulties or delays in the product development process; Jade’sproduct candidatesmay be delayed to a point where they are not commercially viable; clinical trial start up,enrollment or regulatory challengesmay occur;challengesassociated with Jade’s dependence on third-party vendors for the development, manufacture and supply of its product candidatesmay occur;Jade may use its capital resources sooner than expected;and the other risks, uncertainties and factors more fully described in Jade’s most recent filings with the Securities and Exchange Commission (including the Quarterly Report on Form 10-Q for the quarter ended June 30, 2026). Should one or more of these risks or uncertainties materialize, or should any of Jade’s assumptions prove incorrect, actual results may vary in material respects from those projected in these forward-looking statements. You should not place undue reliance on forward-looking statements in this communication, which speak only as of the date they are made and are qualified in their entirety by reference to the cautionary statementsherein. Jade does not undertake or accept any duty torelease publiclyany updates or revisions to any forward-looking statements.This communication does not purport to summarizeall of the conditions,risks and other attributes of an investment in Jade. MA R KE T A ND I ND US TR Y DA T A Certain information contained in this presentation and statements made orally during this presentation relate to or are based on studies, publications and other data obtained from third-party sources as well as our own internal estimates and research. While we believe these third-party sources to be reliable as of the date of this presentation, we have not independently verified, and make no representation as to the adequacy, fairness, accuracyor completeness of, any information obtained from third party sources. Forecasts and other forward-looking information obtained from these sources are subject to the same qualifications and uncertainties as the other forward-looking statements in this presentation. Statements as to our market and competitive position data are based on market data currently available to us, as well as management’s internal analyses and assumptionsregardingthe company, which involve certain assumptions and estimates. These internal analyses have not been verified by any independent sources, and there can be no assurance that the assumptions or estimates areaccurate. While we are not aware of any misstatementsregardingour industry data presentedherein, our estimates involve risks and uncertainties and are subject to change based onvarious factors. As a result, we cannot guarantee the accuracy or completeness of such information contained in this presentation.This presentationcontainscomparisons of data across separate, non-head-to-head studies. No head-to- head study has been conducted comparing JADE101, JADE201 or JADE301 to other candidates or approved agents. Differences may exist between study designs, patient characteristics and other factors, and caution should be exercised indrawing any conclusions from a comparison of the data across studies as cross-study comparisons are inherently limited and such data may not be directly comparable. In addition, data from third party products have been extracted via digitization and represent approximate values. 2
Page 3
PR O GR A M MO A PR E CL I NI CA L PH A S E 1 PH A S E 2 PH A S E 3 PO T EN T IA L IN DI CA T IO NS JADE101 anti-APRIL IgAN JADE201 anti-BAFF-R Multiple systemic AI diseases JADE301 anti-IFN-β Dermatomyositis Advancing potentially best-in-class therapies for autoimmune diseases CO MPA NY OV ERV IEW Well-funded through multiple upcoming milestones; runway into the fourth quarter of 2028 Notes: Jade has entered into exclusive license agreements with Paragon Therapeutics for JADE101, JADE201 and JADE301. AI – Autoimmune; IgAN - IgA nephropathy; BAFF-R – B cell-Activating Factor Receptor; IFN-B – Interferon Beta; MoA – Mechanism of Action 3 Candidates designed to maximize clinical activity and allow patient friendly, infrequent dosing Development candidates from Paragon JA DE 101 ▪ Interim Phase 2 Data: 2027 ▪ Phase 3 Initiation: 1H 2027 JA DE 2 0 1 ▪ Interim Phase 1 Data: 2027 JA DE 301 ▪ Phase 1 Initiation: 4Q 2026 ▪ Interim Phase 1 Data: 2H 2027 Expected Milestones:
Page 4
JADE101 A potentially best-in-class anti- APRIL mAb for IgAN 4
Page 5
0 50,000 100,000 150,000 I gA N E S T . PR E VA L E NC E Require Treatment No Additional Treatment Required IgAN is a $20B+ potential market in the U.S. alone ~169K+ IgAN patients in the U.S., with 60-75% requiring treatment per international guidelines ~1M+ global patients, significant ex-U.S. market potential Notes: Per KDIGO guidelines, treatment should be initiated in all cases where patients have proteinuria ≥0.5 g/day. U.S. prevalence estimate from Food and Drug Administration (FDA); EU prevalence estimate from European Medicines Agency (EMA); Japan / China prevalence estimates from a Novartis presentation. Estimated pricing of ~$360K-$390K per year based on Voyxact. Sources: 2023 Pitcher (CJASN); FDA Reviews for Filspari / Tarpeyo; EMA; Novartis data publicly disclosed; 2018 Schena (Seminars in Nephrology); Reuters U.S. – United States; E.U. – European Union 5 JA DE101 169 205 103 783 0 200 400 600 800 1,000 1,200 I gA N E S T . PR E VA L E NC E U.S. E.U. Japan China ‘000 Patients 1,260
Page 6
High lifetime risk of end-stage kidney disease A need for effective and convenient therapies for lifelong treatment ▪ IgAN is typically diagnosed in young adults between the ages of 16 and 35; higher proteinuria is associated with greater risk of kidney failure ▪ Lifetime risk of progression to end-stage kidney disease begins at low proteinuria thresholds. Notes: Per KDIGO guidelines, treatment should be initiated in all cases where patients have proteinuria ≥0.5 g/day. Sources: 2023 Pitcher (CJASN); 2018 Schena (Seminars in Nephrology); Reuters; American Kidney Fund(Accessed May 2026) 6 JA DE101 IgAN is a progressive autoimmune kidney disease requiring lifelong treatment, with significant need for well-tolerated, disease- modifying therapies that offer convenient dosing.
Page 7
Updated KDIGO guidelines position the anti -APRIL class as the foundational therapy in IgAN KDIGO updates: ▪ Expected to increase IgAN diagnosis ▪ Expand at-risk patient population requiring treatment ▪ Lower proteinuria treatment target to <0.5 g/day, preferably <0.3 g/day ▪ Require targeted therapies that reduce pathogenic IgA Sources: KDIGO Commentary 2026; KDIGO 2025 Guidelines; 2023 Mathur (NEJM); Jade analysis. KDIGO – Kidney Disease Improving Global Outcomes; APRIL – A Proliferation-Inducing Ligand; IgA – Immunoglobulin A 7 JA DE101 Drivers of nephron loss In all patients these should be addressed simultaneously Reduce pathogenic forms of IgA and IgA immune complex formationTreatment strategies IgAN patients at risk of progressive kidney function loss Manage the IgAN- specific drivers for nephron loss Manage the generic response to IgAN- induced nephron loss Cardio- vascular risk reduction Reduce glomerular hyperfiltration and the impact of proteinuria on the tubulointerstitium Blood pressure control Reduce glomerular inflammation B cell modulators, including APRIL inhibitors
Page 8
Reducing pathogenic IgA production by plasma cells B cell depletion or reduction is ineffective in IgAN… ▪ B cell depletion with rituximab (anti -CD20) failed to reduce Gd -IgA1, anti-Gd-IgA1 autoantibody, or proteinuria and did not impact eGFR ▪ B cell suppression with BAFF neutralization (blisibimod) did not reduce IgA or proteinuria …while targeted plasma cell modulation is highly effective ▪ APRIL and dual APRIL/BAFF neutralization result in significant and sustained depletion of Gd -IgA1, reduction in proteinuria, and eGFR stabilization A potentially disease-modifying approach for IgAN Neutralizing APRIL depletes Gd-IgA1, reduces proteinuria, and preserves eGFR, providing a disease- modifying treatment of IgAN without impacting B cell development and maturation JA DE101 Sources: 2024 Cheung (Front Nephrol); 2023 Mathur (J Clin Med) Gd-IgA1 – Galactose-deficient immunoglobulin A1; eGFR – Estimated glomerular filtration rate; BAFF – B-cell activating factor 8 HSC Pro B cell Large pre-B cell Small pre-B cell Immature B cell Mature Naïve B cell Memory B cell Plasma cell B O NE MA R R OW M U C OS A M UC OS A & B O NE MA R R OW *Gradient indicates level of receptor expression C D 2 0 E X PR E SS IO N A P R I L D E P EN D EN C Y B A F F D EP EN D E NC Y APRILAPRIL blocking therapy Plasma cell differentiation Antibody class -switching H IT 1 Production of galactose - deficient IgA1 (Gd -IgA1) H IT 2 Synthesis of anti -Gd- IgA1 autoantibodies H IT 3 Autoantibodies bind Gd - IgA1 to form p athogenic immune complexes H IT 4 Deposition of immune complexes in the mesangium and initiation of kidney injury
Page 9
Phase 3 IgAN data have not demonstrated additional patient benefit from dual APRIL/BAFF vs selective APRIL inhibition Study populations were representative of high-risk, global IgAN patients Sibeprenlimab UPCR Δ from baseline (%, 9 months) Δ -51.2% (p < 0.0001) Povetacicept UPCR Δ from baseline (%, 9 months) Δ -49.8% (p < 0.0001) Atacicept UPCR Δ from baseline (%, 9 months) Δ -41.8% (p < 0.0001) Notes: Information provided above is for illustrative purposes only and no head-to-head clinical trials have been conducted. Differences exist between study or trial designs and subject characteristics, and caution should be exercised when comparing data across trials. Data digitized from graphs where publications did not provide specific values. Sources: Perkovic et al. ERA 2025 (sibeprenlimab), ORIGIN Phase 3 clinical trial (atacicept, NCT04716231), RAINIER Phase 3 (povetacicept, NCT06564142). UPCR – Urine Protein-to-Creatinine Ratio; Δ – Delta 9 JA DE101 S E LE CT I VE A NT I-A PR I L D UA L AP RI L / B AF F 2.1 -50.2 P L AC E B O N= 1 6 8 S I B E P R E NL I M A B N= 1 5 2 -6.8 -45.7 A T A CI C E P T N= 1 0 3 P L AC E B O N= 9 5 -4.3 -52.0 P O V E T AC I C E P T N= 1 3 1 P L AC E B O N= 6 8
Page 10
Half-life extension through validated YTE Fc modification ▪ Longer exposure intended to maximize clinical activity and reduce dosing interval to no more frequently than every 8 weeks Potentially best-in-class properties of JADE101 Fully-human, ultra-high binding affinity, and extended half-life Notes: Jade and its licensor, Paragon, havefiled patent applications covering the subject matter of JADE101. No head-to-head clinical trials have been conducted between JADE101 and the referenced drug candidates. Cross-trial comparisonsare inherently limited and presented for hypothesis-generating purposes only. Sources: Internal SPR data; Evans, 2023 (Povetacicept); Benchmarks manufactured based on publicly available sequences. Fc – Fragment crystallizable receptor; fM – Femtomolar; mAb – Monoclonal Antibody 10 Ultra-high (fM) APRIL binding affinity ▪ Binds APRIL to neutralize activity ▪ Selective to APRIL to avoid unnecessary immune suppression ▪ Greater APRIL binding affinity than sibeprenlimab (~750x), zigakibart (~2,000x), and povetacicept (~20x) Novel epitope discovered through de novo campaign to achieve first fully-human, potentially best-in-class anti- APRIL mAb JA DE101
Page 11
IgA responses are consistent between HVs and IgAN patients and predictive of clinical activity JA DE101 Notes: Sibeprenlimab Phase 2 (intravenous, IV) and Phase 3 (subcutaneous) IgAN data are included. Phase 2 data are averages of the 4 mg/kg and 8 mg/kg cohorts (HV IV data is from the 6 mg/kg group); the two cohorts saw effectively equivalent IgA reduction at weeks 2, 4, and 8. Zigakibart UPCR data is at W52. Datapoints extracted via digitization and represent approximate values. The company does not possess the underlying raw third-party data. Trend lines are best linear fit. These data are derived from different trials at different points in time, with differences in methodology, design and populations. Caution should be exercised in drawing any conclusions from a comparison of the data across studies as cross-study comparisons are inherently limited and such data may not be directly comparable. Sources: 2025 Gufford (ASN Presentation); Voyxact 2025 HV – Healthy Volunteer; W – Week; BSL – Baseline; CHG – Change; PTS – Patients 11 60 0 20 0 60 0 20 0 60 0 20 0 60 0 20 0 wk wk wk wk wk wk wk wk wk2 wk wk6 wk wk2 wk2 wk2wk2 wk2 wk wk wk wk IgA reduction in HVs is highly correlated with IgA reduction in IgAN patients at multiple time points… …and early IgA reduction further correlates with W36 UPCR reduction, in IgAN patients MEAN % C HG FR O M BSL I N I gA I N I gAN PT S MEAN % C HG FRO M BSL I N I gA I N HV S MEAN I gA % R EDUC T I ON (W EEK 8) G EOMETRI C MEAN UP C R % REDUC TI ON (W EEK 36) r=0.98 r=0.92 igakibart PovetaciceptSibeprenlimabSibeprenlimab Placebo Treatment Group ezagitamab FelzartamabTelitaciceptTelitacicept Placebo igakibart PovetaciceptSibeprenlimabSibeprenlimab Placebo Treatment Group
Page 12
JADE101 Interim Phase 1 Data 12
Page 13
JADE101 Phase 1 study met or exceeded objectives JA DE101 Clinical data support potential for every-12-week subcutaneous dosing with best-in-class, disease- modifying potential Notes and Sources: Data cutoff – April 14, 2026. Data on sibeprenlimab (Sibe) and povetacicept (Pove) from third-party data; Reported half-life of Sibe 9.3 days (Voyxact, 2025) and Pove 2.8 days (Davies, 2024). Sibe TMDD threshold based on a visual estimate of third -party data. No head-to-head study has been conducted comparing JADE101 to other candidates or approved agents. Differences exist between study designs, patient characteristics and other factors, and caution should be exercised in drawing any conclusions from a comparison of the data across studies as cross-study comparisons are inherently limited and such data may not be directly comparable. SC – Subcutaneous; TMDD – Target-Mediated Drug Disposition; ADA – Anti-Drug Antibodies; PK – Pharmacokinetics; PD – Pharmacodynamics; fAPRIL – Free A Proliferation-Inducing Ligand; Q8W – Every 8 Weeks; Q12W – Every 12 Weeks 13 EN DPO INT JADE1 01 O BJECTIVE Dosing ▪ Single SC maintenance dose Q8W Safety ▪ Favorable safety profile consistent with selective anti- APRIL mechanism Pharmacodynamics ▪ ≥55% IgA reduction sustained for ≥ weeks ▪ Rapid, complete and sustained suppression of fAPRIL Pharmacokinetics ▪ Extended half-life ▪ TMDD mitigation ▪ Minimal ADA impact on exposure JADE1 01 DATA Potential for single SC maintenance dose Q12W Favorable safety profile; well-tolerated at all tested doses ~70% IgA reduction sustained at 12 weeks at 700 mg; modeled to be maintained with single SC 350 mg Q12W maintenance dose IgA-lowering potency ~379-fold higher than sibeprenlimab; ~26-fold higher than povetacicept Rapid, complete and sustained suppression of fAPRIL ~8.7-fold longer half-life than povetacicept; ~2.6-fold longer than sibeprenlimab TMDD threshold estimated ~2.5-fold lower than sibeprenlimab No apparent impact of ADA observed on PK or PD
Page 14
JADE101 Phase 1 study ongoing DE S IG N ▪ Randomized, double -blind, placebo - controlled ▪ Single ascending dose ▪ Subcutaneous administration (175 mg/mL) PO PUL A T IO N ▪ 32 healthy adult volunteers ▪ N=8 per cohort (6:2 active:placebo ) O BJE C TI VE S ▪ Primary: Safety and tolerability ▪ Secondary: Pharmacokinetics ▪ Exploratory: Pharmacodynamics (APRIL, IgA, immunoglobulins); Immunogenicity Dose levels and length of follow-up to date PH ASE 1 1 7 5 MG SC : N = 6 :2 Follow-up: ~8 months 3 5 0 MG SC : N = 6 :2 Follow-up: ~7 months Planned maintenance dose in Phase 2 and Phase 3 7 0 0 M G SC : N = 6 :2 Follow-up: ~6 months Planned induction dose in Phase 2 and Phase 3 1 ,4 0 0 MG SC : N = 6 :2 Follow-up: ~5 months Notes: ClinicalTrials.govID: NCT07059312.Numbers presented as subjects receiving JADE101 relative to placebo. Each cohort included a sentinel group, n = 2 (1 JADE101, 1 placebo); remainder dosed after safety clearance. 14
Page 15
Baseline characteristics were typical of healthy volunteers PH ASE 1 Notes: Data cutoff – April 14, 2026. BMI – Body Mass Index; SD – Standard deviation 15 JA DE 101 A ND PL A C EB O 175 MG 3 5 0 M G 700 MG 1 , 4 0 0 M G A L L C OH O RT S N 8 8 8 8 32 Age, (yr), Mean (SD) 38.0 (7.86) 44.5 (9.87) 28.0 (9.04) 37.6 (13.70) 37.0 (11.51) Female N (%) 2 (25) 6 (75) 3 (38) 5 (63) 16 (50) White N (%) 5 (63) 6 (75) 4 (50) 3 (38) 18 (56) Asian N (%) 2 (25) 1 (13) 3 (38) 1 (13) 7 (22) BMI, (kg/m2) Mean (SD) 25.5 (2.70) 26.7 (2.88) 25.9 (3.05) 24.2 (3.25) 25.6 (2.97)
Page 16
JADE101 demonstrated favorable safety profile and was well tolerated across all evaluated doses ▪ No severe AEs or deaths ▪ All TEAEs were mild/moderate in severity ▪ No clinically significant changes in ECGs or vitals ▪ No trends of signals in safety labs ▪ No cases of IgG ≤3 g/L ▪ Well-tolerated locally by SC injection ▪ 3/32 (9%) mild (2)/moderate (1) injection site erythema ▪ 1/32 (3%) mild injection site pain ▪ No apparent impact of anti-drug antibodies was observed on PK or PD Healthy Volunteer SAD Safety Summary PH ASE 1 JA DE 101 A ND PL A C EB O 1 7 5 M G 3 5 0 M G 700 MG 1400 MG A L L C OH OR T S N 8 8 8 8 32 ≥ 1 TEAE, n (%) 6 (75) 6 (75) 5 (63) 7 (88) 24 (75) ≥ 1 SAE, n 0 0 0 0 0 ≥ 1 severe TEAE, n 0 0 0 0 0 Discontinued due to AE 0 0 0 0 0 TEAEs in the pooled safety analysis occurring in > 2 participants were headache (25%), upper respiratory tract infection (21.9%); injection site erythema, oropharyngeal pain, and pyrexia (9.4% each) Notes: Data cutoff – April 14, 2026. AE – Adverse event; ECG – Electrocardiogram; SAD – Single Ascending Dose; SAE – Serious Adverse Event; TEAEs – Treatment Emergent Adverse Events 16
Page 17
JADE101 single dose IgA reductions exceeded those reported with first-generation molecules 17 Notes and Sources: Data cutoff – April 14, 2026. Internal data; IgA responses estimated via noncompartmental analysis of individual JADE101 profiles and internal analyses of mean reported profiles of povetacicept (Davies, 2024) and sibeprenlimab (Mathur, 2022; Zhang, 2023). Povetacicept and sibeprenlimab data points extracted via digitization and represent approximate values. The company does not possess the underlying raw third-party data. No head-to-head study has been conducted comparing JADE101 to other candidates or approved agents. Differences exist between study designs, patient characteristics and other factors, and caution should be exercised in drawing any conclusions from a comparison of the data across studies as cross-study comparisons are inherently limited and such data may not be directly comparable. First-gen – First Generation ▪ Prolonged IgA reductions of ~70% following a single dose of JADE101 ▪ Reductions exceeded those reported for first-gen agents ▪ Induction dose of 700 mg expected to drive ~70% IgA reductions, with 350 mg maintenance dose predicted to sustain this reduction ▪ Largest reported magnitude of IgA lowering effect with a single dose for an anti-APRIL or dual APRIL/BAFF ▪ IgA reductions sustained at12 weeks at 700 mg PH ASE 1 10 0 10 30 50 0 0 12 16 20 2 2 32 1 5 mg 350 mg 00 mg 1 00 mg Placebo MEAN I gA C F B ( %) N OMI NAL TI ME (W EEK) 0 60 50 0 30 20 ommercial Dose Phase 3 Dose IgA Change from Baseline by Dose IgA reduction in Healthy Volunteers MEAN I gA C F B ( %) SI B E PR E NL I MA B P OV ET A C IC E PT J A D E 10 1 700 mg single dose predicted to reflect IgA responses with Q12W maintenance dosing (700 mg induction + 350 mg maintenance)
Page 18
0.001 0.01 0.1 1 10 100 1000 0.01 0.1 1 10 100 1000 Sibe Ziga Pove JADE101 R2 = 0.9 ▪ Ultra-high APRIL binding affinity predicted JADE101’s enhanced in vivo potency to lower serum IgA in humans ▪ JADE101 has shown rapid, deep and sustained IgA depletion JADE101 demonstrated compelling in vivo potency to lower IgA PH ASE 1 APR I L KD( pM) I gA EC 50 (ηM) J ADE101 POVE SIBE ZIG A IgA EC50 (nM) 0.010 0.27 3.9 16.4 IgA EC50 v JADE101 n/a 27x 379x 1,595x Dosing Interval Potentially Q12W Q4W Q4W Q2W Notes and Sources: Data cutoff – April 14, 2026. Internal data; Evans, 2023 (Pove); Benchmarks manufactured based on publicly available sequences. IgA EC50 estimates calculated using compartmental PK models linked to indirect response models to describe IgA kinetics built using JADE101 -01 data or published PK and IgA concentration-time profiles in single dose studies and demonstrated maximum biological effects (Sibe: FDA Review 2025) Sibe (Mathur, 2022; Zhang, 2023); Ziga (Kooienga, 2025); Pove (Davies, 2024); Data points extracted via digitization and represent approximate values. The company does not possess the underlying raw third-party data. These data are derived from different trials at different points in time, with differences in trial design and populations. No head -to-head clinical trials of JADE101 and other agents have been conducted. EC – Effective Concentration; V – Value; nM – Nanomolar 18 (Q2W) (Q4W) (Q4W) Potentially Q12W APRIL Binding Affinity and IgA Lowering Potency
Page 19
0 -10 -30 -50 -70 0 8 16 24 32 40 48 JADE101 350 mg SC Q12W maintenance Pove 80 mg SC Q4W Sibe 400 mg SC Q4W JADE101 PD modeling supports Q12W maintenance dosing Deeper IgA reductions simulated over first-generation anti-APRILs ▪ JADE101 induction dose (700 mg) predicted to rapidly maximize IgA depletion ▪ >70% IgA reductionsprojected at steady state with a single subcutaneous maintenance injection (350 mg) every12 weeks ▪ IgA reductions modeled to be faster and deeper than first generation anti- APRIL or dual APRIL/BAFF PH ASE 1 Notes and Sources: Data cutoff – April 14, 2026. Internal data; Solid lines represent the median and shaded area represents the 5th and 95th prediction intervals across 500 simulated trials. JADE101 population-based simulations informed by interim biomarker rich healthy volunteer data obtained in JADE101-01 integrated with data available in the public domain. Sibeprenlimab and povetacicept simulations conducted via population-based approaches using internal models informed by data available in the public domain (Pove: Davies 2024; Sibe: FDA Review 2025). Underlying povetaciceptand sibeprenlimabdata points extracted via digitization and represent approximate values. The company does notpossess the underlying raw third-party data. Modeled data may not be realized in actual clinical studies and may not accurately represent performance of third-party products. 19 JADE101 Q12W Dosing (Year 1) 700 mg Induction 350 mg Maintenance PR ED IC T ED I gA C FB ( %) TI ME ( W EEK) Simulated IgA vs Time – 48 weeks
Page 20
Pharmacokinetics fAPRIL 1 5 mg 350 mg 00 mg 1 00 mg Placebo JADE 101 CO NC . ( μg/ m L) 0.001 0.01 0.1 1 10 100 0 12 16 20 2 IgA reductions for 12 weeks enabled by dose-dependent PK and rapid, complete, and sustained fAPRIL suppression Notes and Sources: Data cutoff – April 14, 2026; Internal data. Half-life dependent on dose and dose interval; JADE101 half-life measured at 700 mg induction dose. Sibeprenlimab TMDD threshold based on visual estimate of third-party data. Duration of fAPRIL response (>90%) estimated via noncompartmental analysis of individual JADE101 participant profiles. No head- to-head study has been conducted comparing JADE101 to other candidates or approved agents. Differences exist between study designs, patient characteristics and other factors, and caution should be exercised in drawing any conclusions from a comparison of the data across studies as cross-study comparisons are inherently limited and such data may not be directly comparable. 20 PH ASE 1 100 5 50 25 0 25 50 0 12 16 20 2 2 32 f APR I L CF B (% ) TI ME ( W EEK) ▪ ~8.7 fold longer half-life than povetacicept; ~2.6 fold longer than sibeprenlimab ▪ JADE101 half-life: 24.2 days ▪ JADE101 TMDD threshold estimated ~2.5-fold lower than sibeprenlimab ▪ PK profiles of first -gen anti-APRIL mAbs strongly influenced by TMDD ▪ Deep serum fAPRIL suppression as rapidly as 2 hours post SC dose administration ▪ >90% APRIL suppression sustained for a median of 85 days at 700 mg TI ME ( W EEK) 1 5 mg 350 mg 00 mg 1 00 mg Placebo
Page 21
Changes in IgG, IgM and IgE were consistent with the selective anti-APRIL MoA IgG IgM ▪ Magnitude of IgG- lowering consistent with relatively IgG- sparing selective- anti-APRIL MoA ▪ No cases of IgG ≤ 3 g/L ▪ Substantial IgM and IgE reductions PH ASE 1 IgE 1 5 mg 350 mg 00 mg 1 00 mg Placebo 10 0 10 30 50 0 0 12 16 20 2 2 32 10 0 10 30 50 0 0 12 16 20 2 2 32 0 50 30 10 0 10 30 50 0 0 12 16 20 2 2 32 I gG C F B ( % ) TI ME ( W EEK) I gM CF B ( %) TI ME ( W EEK) I gE C FB ( %) TI ME ( W EEK) Notes and Sources: Data cutoff – April 14, 2026; Internal JADE101-01 data. IgG – Immunoglobulin G; IgM – Immunoglobulin M; IgE – Immunoglobulin E 21
Page 22
JADE101 Next steps 22
Page 23
▪ Plan to evaluate two dosing regimens (Q12W and Q8W) in Phase 2 and Phase 3 ▪ Two dose Phase 3 may enable an accelerated Phase 3 initiation without awaiting Phase 2 data ▪ Supports global regulatory expectations for dose -finding ▪ Initial induction dose intended to drive ~70% IgA reductions at earlier timepoints ▪ Induction dose is 700 mg, followed by Q12W or Q8W maintenance dosing (350 mg) beginning at Week 4 Q12W dosing expected to optimize clinical activity and convenience for patients N EX T ST EPS YE A R 1 YE A R 2 JADE101 Q12W Pove/Sibe Q4W Ataci/Ziga QW/2W 23 Notes: JADE101 projected dosage frequency based on internal population pharmacodynamic modeling anddosing schedules remain subject to further clinical investigation.No head-to-head study has been conductedcomparing JADE101 to other candidates orapproved agents. Differences exist between studydesigns, patient characteristics and otherfactors, and caution should be exercised in drawing anyconclusions from acomparison of thedata across studies as cross-study comparisons are inherentlylimited and such data may not bedirectly comparable.
Page 24
JADE101 Phase 2 IgAN patient trial initiated; interim data anticipated in 2027 DE S IG N ▪ Randomized, open -label ▪ Subcutaneous administration PO PUL A T IO N ▪ Adults with IgAN within 5 yrs ▪ Proteinuria ≥0. 5 g/g ▪ eGFR ≥30 mL/min/m 2 ▪ Stable SO ≥12 weeks O BJE C TI VE S ▪ Safety and tolerability ▪ UPCR-24 over time (<0.5 g/day, <0.3 g/day) ▪ eGFR over time N EX T ST EPS WEE K 0 Induction Dose 700 mg Q 8W ( N = ~ 1 5) 3 5 0 M G (to Week 100) WEE K 4 Maintenance Dosing 350 mg Q 12 W ( N = ~ 15 ) 3 5 0 M G (to Week 100) Safety Follow-Up 24 weeks after last dose Notes: ClinicalTrials.govID: NCT07541287 SOC – Standard of Care 24 Open-label ExtensionOr
Page 25
JADE201 a potentially best-in-class afucosylated anti-BAFF-R mAb 25
Page 26
A potentially best-in-class afucosylated anti-BAFF-R mAb ▪ B cell depletion has proven effective in autoimmune disease, but existing therapies like rituximab and anti -CD19 agents face limits: ▪ Resistance mechanisms, particularly elevated BAFF after anti-CD20 therapy, enable autoreactive B cells to repopulate, undermining durability ▪ Ianalumab, an afucosylated anti- BAFF-R, provided proof-of- concept for overcoming these barriers, including clinical tissue B cell depletion4 With dual MOA B cell depletion to treat autoimmune diseases JADE201 builds on ianalumab’s proof-of-concept, adding HLE for expected improved durability, less frequent dosing, and potentially best-in-class profile JA DE201 Sources: 1. Merino-Vico Euro J Immunol 2023; 2. Ramwadhdoebe Rheumatology 2019; 3. Daneshvar E Int J Derm 2023; 4. Cornec, ACR Convergence 2025. HLE – half-life extension 26 Incomplete B cell depletion due to low target receptor expression on some B cell subsets or paucity of effector cells to mediate killing1 Residual B cells in secondary lymphoid tissues and/or ineffective depletion of B cells in ectopic lymphoid tissue after treatment2 Sparing pathogenic autoantibody producing cells, including plasmablasts Resistance mechanisms, including increased BAFF expression following treatment with rituximab3
Page 27
JADE201's dual MOA expected to deliver deeper, more durable B cell depletion Direct Cytotoxicity via Enhanced Effector Function ▪ Validated mechanism that induces rapid B cell depletion ▪ Enhanced cytotoxicity by ADCC ▪ Potent depletion of circulating B cells B Cell Inhibition and Depletion by BAFF Starvation ▪ Mechanism works in context of low receptor expression ▪ Relevant in secondary and ectopic lymphoid tissues where effector cells may be scarce ▪ Avoids B cell repopulation and resistance due to increased BAFF expression following B cell depletion with anti-CD20 agents JA DE201 ADCC – antibody-dependent cellular cytotoxicity 27 N K C E L L B CE L L 1. ADCC B CE L L 2. BAFF Starvation Fc-R BAFF-RJADE201 BAFF BAFF-R JADE201 Survival
Page 28
afucosylated for enhanced ADCC Binds BAFF-R broadly expressed on B cells ▪ Enhanced ADCC activity on B cells similar to ianalumab ▪ Blocks BAFF activity similar to ianalumab HLE via Fc LS mutation ▪ Predicted to match, with potential for improved clinical activity due to increased exposure compared to ianalumab with less frequent dosing Potentially best-in-class properties of JADE201 Novel IP for composition of matter into mid-2040s Notes: Jade and its licensor, Paragon, have filed patent applications covering the subject matter of JADE201. No head-to-head clinical trials have been conducted between JADE201 and the referenced agent. 28 JA DE201
Page 29
JADE201 exhibits high BAFF-R binding affinity and functional activity in preclinical studies BAFF-R Binding (HEK Cells) BAFF-R Blockade (Competition ELISA) JA DE201 ADCC Activity Primary human CD19+ B Cells Additional Attributes Similar Between Clones ▪ Affinity to human/cyno BAFF -R by SPR ▪ BAFF-R binding (Raji B cells) ▪ FcR binding (excluding FcRn*) ▪ C1q binding ▪ ADCC activity on Raji B cells Note: No head-to-head clinical trials of JADE201 and the referenced agent have been conducted. Ianalumab manufactured from publicly available sequence. *LS mutation ~10x higher affinity to FcRn. ELISA – Enzyme-linked immunosorbent assay; HEK – Human Embryonic Kidney cell; Cyno – Cynomolgus macaque; pM – Picomolar; SPR – Surface plasmon resonance; C1q – Complement component 1q 29 1 10 100 20 0 20 0 60 0 100 120 ianalumab JADE201 2.01 I 50(n ) 2.0 0.0001 0.01 1 100 0 5000 10000 15000 ianalumab JADE201 1.65 E 50(n ) 1. MF I AB C O NC . ( nM ) I NH I BIT I O N% AB C O NC . ( nM ) 0 0 10 100 1000 10 100 1000 0 1000 2000 3000 edia ehicle (0.1% P S) ianalumab JADE201 LI VE B CELL S ( C OU NT ) AN TI BO DY CO NC EN TRATI O N ( pM )
Page 30
BAFF-Receptor Occupancy (RO) 0 20 0 20 0 60 0 100 120 JADE201 demonstrates deep B cell depletion in NHPs JADE201 PK JADE201 demonstrates dose-dependent PK. Rapid RO observed with complete RO achieved at doses above 1 mg/kg Deep and sustained B cell depletion achieved after single dose of JADE201 in NHPs JA DE201 B Cell Depletion NHP – Non-human primates; RO – Receptor occupancy 30 10 2 10 1 100 101 102 103 10 105 106 JADE 201 CO NC EN T RAT I O N ( NG / ML )TI MEPO I NTS BAF F R O ON B C ELLS ( % MEAN ±SEM ) TI ME P OS T -TR EATMENT MEAN ( ±SEM) B C ELL DENS ITY ( C OUN T/ UL) C FB ( %) T I MEPO I NT S 0 20 0 60 0 100 120 1 0 0.001mg/kg 0.01mg/kg 0.1mg/kg 1mg/kg 10mg/kg
Page 31
HLE has potential to provide sustained BAFF receptor occupancy and improved clinical response JADE201 demonstrates a differentiated NHP PK profile from ianalumab >2X HLE demonstrated in NHPs JA DE201 JADE201 NHP t1/2 = 5.4 days t1/2 = 2.7 days Notes: Individual NHP time points that appear to be impacted by ADA excluded from half-life determinations and mean concentration-time plots. Information provided above is for illustrative purposes only and no head-to-head clinical trials have been conducted. Ianalumab manufactured from publicly available sequence. Sources: 12019 Dorner (Ann Rheum Dis) 31 ▪ Ianalumab has an observed human T 1/2 ~ 10 days1 ▪ JADE201 with HLE has the potential to provide complete BAFF-R coverage for an extended duration ▪ Potential for deeper, more durable clinical responses ▪ Extended dosing interval providing a more convenient, infrequent SC dosing profile 0.01 0.1 1 10 100 1000 0 1 2 2 56 Ianalumab, 30 mg/kg I JADE201, 30 mg/kg I N OMI NAL T I ME (D AY) MEAN ( +SD) C ON CEN T R AT IO N ( μG /ML)
Page 32
JADE201 first-in-human trial underway; interim data expected in 2027 Phase 1 Study Design Randomized, double -blind, placebo-controlled SAD study SC administration in adults (n=36) with rheumatoid arthritis. Objectives PR IM A R Y ▪ Safety and tolerability S E CO ND A RY & E XP LO R AT O RY ▪ Pharmacokinetics ▪ Pharmacodynamics ▪ Immunogenicity ▪ B cell depletion ▪ DAS28 JADE201 preclinical profile supports potential for best-in-class clinical activity with convenient, patient-friendly dosing S C D OS E 1 : N = 5: 1 S C D OS E 2: N = 5: 1 S C D OS E 3 : N = 5: 1 S C D OS E 4 : N = 5 : 1 Notes:Numbers presented as subjects receiving JADE201 relative to placebo. Each cohort to include a sentinel group, n = 2 (1 JADE201, 1 placebo); remainder dosed after safety clearance. DAS – Disease Activity Score 32 JA DE201 S C D OS E 5 : N = 5: 1 S C D OS E 6 : N = 5 : 1
Page 33
JADE201 profile could enable broad opportunity in multiple indications where B cells are pathogenic JA DE201 Notes: 1) Representative of potential best-in-class and first-in-class JADE201 indications; 2) Illustrative representation of proportion of moderate-to-severe disease vs. refractory patients across B cell implicated autoimmune diseases Tx – Treatment; TCEs – T-cell Engagers; BiTEs – Bispecific T-cell Engagers; CAR-Ts – Chimeric Antigen Receptor T-cell Therapies; CAR-NKs – Chimeric Antigen Receptor Natural Killer; ANCA – Antineutrophil cytoplasmic antibodies; IV – Intravenous 33 TCEs & Cell Therapies e.g., BiTEs, CAR-Ts, CAR-NKs U.S. Disease Prevalence1 Disease severity and key Tx modalities across indications2: Sjögren’s Disease ~3.5M Lupus Nephritis ~85,000 Immune Thrombo- cytopenia ~85,000 Primary Membranous Nephropathy ~35,000 ANCA- Associated Vasculitis ~125,000 Bullous Pemphigoid ~40,000 JADE201 core opportunity Best-in-class potential First-in-class BAFF-R Moderate-to-severe Refractory JADE201 anti-BAFF-R mAb Addresses later-line and highly refractory disease Targets MoA validated across multiple indications in late - stage trials Proven efficacy and MoA target CD20/CD19 B cell depleters e.g., rituximab, obinutuzumab Cell therapy Tx could lead to full immune reset Potential for improved benefit / risk vs. B cell depleters Safety limitations, incl. high infection risk and black box Low applicability to majority of moderate-to-severe disease Potential for better durability with greater tissue depletion and blockade of resistance Limited durability, with relapse and re-treatment over time High treatment burden, incl. IV admin and safety considerations Burdensome IV admin and dosing schedule Designed for improved dosing convenience
Page 34
JADE301: IFN-β Neutralizing mAb for Dermatomyositis (DM) 34
Page 35
Dermatomyositis is a debilitating autoimmune disease affecting ~50K U.S. adults ▪ Affects adults and children, with higher prevalence in women ▪ 60–80% of patients do not achieve sustained remission ▪ Mortality ~3X the general population Sources: Myositis Support and Understanding Association; Pfizer Pipeline Day, Dec 2022; 2010 Bendewald (JAMA Dermatol); 2012 Marie (Curr Rheumatol Rep); 2023 Kleitsch (Arch Dermatol Res) QoL – Quality of Life; CV – Cardiovascular 35 JA DE301 37% unable to climb one flight of stairs A chronic, multisystem disease High impact on daily activities 53% unable to walk >one mile 50% unable to bend, lift or stoop Potential lung, CV and malignancy-related complications Proximal muscle weakness and functional impairment Painful inflammatory skin disease 58% experience severe itch; results in sleep disruption for many patients
Page 36
Current care is steroid-dependent and burdensome ▪ Steroids are used in ~80% of DM patients and come with significant side effects ▪ Treatment depends on severity of clinical presentation, organ involvement, and autoantibody type ▪ High residual disease burden: Nearly all patients experience pain, >50% require opioids ▪ Despite existing therapies, most adults with DM experienced at least one disease flare in the past year Therapies Received by ~34K Treated Dermatomyositis Patients IVIG, only FDA-approved DM therapy requires inconvenient multi-day monthly IV infusions and comes with significant toxicity Opportunity for a targeted, disease- modifying and steroid-sparing therapy with durable control and convenient, infrequent SC administration Sources: Octagam 10% Dosing & Admin Guide, Pfizer; Octagam 10% Prescribing Info; 2023 Bhashyam (Rheumatol); Roivant Brepocitinib Investor Event June 2025; Priovant Corporate Presentation, Feb 2025 DM – Dermatomyositis; IVIG – Intravenous immunoglobulin; IST – Immunosuppressive therapy; FDA – Food & Drug Administration 36 JA DE301 24% 34%6% 15% 18% 3% Only Steroids Steroids + IST Steroids + Biologic/IVIG Steroids + IST + Biologic/IVIG Only ISTs All Other Regimens
Page 37
Half-life extension through validated YTE Fc modification Effector-null fully human IgG1 Fc Binds IFN-β with higher affinity than existing therapies Potentially best-in-class properties of JADE301, an IFN-β neutralizing mAb Notes: Jade's licensor, Paragon, has filed patent applications covering the subject matter of JADE301. No head-to-head clinical trials have been conducted between JADE301 and existing therapies. IgG1 Fc – Immunoglobulin G Subclass 1, Fragment Crystallizable 37 JA DE301 Predicted differentiated SC dosing for patient convenience Novel anti-IFN-β mAb from a de novo antibody discovery campaign
Page 38
IFN-β is a key driver of skin and muscle disease in DM Excess IFN-β can amplify inflammation, impair muscle repair and contribute to tissue damage ▪ Type I interferon signaling is markedly overactive in DM skin and muscle ▪ Excess signaling activates immune cells, impairs muscle repair and disrupts microvasculature ▪ IFN-β is the predominant type I interferon elevated in DM blood and skin ▪ Autoantibodies further drive expression by targeting regulators of IFN-β ▪ Serum IFN-β, but not IFN-α, correlates with skin disease activity ▪ Therapeutic IFN-β exposure has been linked to new-onset or worsening DM- like disease Sources: 2005 Greenberg (Ann Neurol); 2025 Bolko (Front in Immunol); 2017 Huard (Br J Dermatol); 2011 Liao (Ann Rheum Dis); 2024 Pinal-Fernandez (Ann Rheum Dis); 2021 Patel (J invest Derm); 2008 Somani (Arch Dermatol); 2015 Kolb-Maurer (Int J Mol Sci) IFN-α – Interferon alfa; IFN-β – Interferon-beta; MPI – Mean Pixel Intensity; HC – Healthy Controls; DAPI – ′,6-diamidino-2-phenylindole (for nuclear staining) 38 JA DE301 HC DM 0 10 20 30 Epidermal IFN-β IFN-β MPI ✱ ✱ ✱
Page 39
JADE301 combines a targeted mechanism with a differentiated molecular profile in DM ▪ Designed to directly inhibit activity of IFN -β, quieting immune activation, muscle and skin damage ▪ Potential disease -modifying therapy in DM ▪ Designed to selectively neutralize IFN -β while sparing other cytokines, including IFN -α ▪ Expected to have better safety profile versus IFNAR blockade, which increases susceptibility to viral infection and reactivation ▪ More specific, with potential for enhanced clinical activity, while avoiding broad inhibition of multiple cytokine-signaling pathways, such as JAK/TYK2 JADE301 designed to selectively neutralize IFN-β and interrupt disease-driving signal Source:Jade internal data IFNAR – Interferon Alpha/Beta Receptor;JAK – Janus Kinase; TYK – Tyrosine Kinase 2 39 JA DE301
Page 40
DAZUKI BAR T MoA anti-IFN-β Status Phase 3 ongoing Absolute Δ in CDASI-A (cutaneous disease activity, W12) Safety Well-tolerated Dosing 600 mg IV, Q4W (~43% F) JADE301 has best-in-class potential for IFN-β, a validated target for DM ▪ Dazukibart Phase 2 data demonstrated best-in- disease improvement in cutaneous disease activity (CDASI), and was well-tolerated ▪ Dazukibart is dosed Q4W, IV ▪ 2% of patients achieved ≥ 0% reduction in DASI ▪ Positive TIS trend in muscle-predominant patients ▪ JADE301 has best-in-class potential ▪ High binding affinity to maximize IFN-β neutralization ▪ SC dosing for convenience ▪ Half-life extension expected to increase exposure and reduce patient burden Sources: 2023 Vleugels (AAD Presentation); 2020 Neelakantan (Clin Pharm); 2022 Aggarwal (NEJM); 2020 Paik (A&R); 2025 Fiorentino D (Lancet); 2025 Fournier (EADV Journal) F – Subcutaneous bioavailability; CDASI – Cutaneous Dermatomyositis Disease Area and Severity Index 40 JA DE301 2.9 16.6 19.2 P L A C E B O 1 5 0 M G 6 0 0 M G N= 1 4 N = 2 8 N= 1 5
Page 41
Selective IFN-β blockade and SC dosing position JADE301 for best-in-disease potential JA DE301 41 Notes: Available competitor Phase 2/3 and label data reflect reported or digitized placebo-adjusted mean or least-squares (LS) mean differences. Dazukibart TIS reflects prespecified sensitivity analysis in muscle full analysis set (FAS); CDASI reflects pooled skin FAS. Information provided above is for illustrative purposes only. Differences exist between study or trial designs, and caution should be exercised when comparing data across trials. No head-to-head clinical trials have been conducted between JADE301 and the referenced therapies. Sources: 2025 Fiorentino (Lancet); Dazukibart Ph 3 (NCT05895786); 2026 Vleugels (NEJM); 2022 Adas (Expert Rev Clin Immunol); Argenx R&D Spotlight June 2026; AstraZeneca H1 & Q2 results July 2026; Saphnelo Prescribing Info; 2022 Aggarwal (NEJM); Octagam 10% Prescribing Info TIS – Total Improvement Score; FcRn – neonatal Fc receptor; nd – no data; “~” – data digitized from graphs where publications did not provide specific values PR O DUC T M EC HAN ISM · RO U TE · ST AGE E F FI CA C Y (PB O-A DJUS T E D) W E EK 1 2 / F U RT HE ST RE P OR TE D S A F E TY DO S IN G C ON VE N IE N CE T IS C DA S I Dazukibart Anti-IFN-β mAb · I · Phase 3 ✓ 20.8 (Ph 2) / nd ✓ -16.3 (Ph 2) / nd ✓ Generally favorable Phase 2 safety profile IV over approx. 1 hour, every 4 weeks Brepocitinib TYK2/JAK1 inhibitor · Oral · Phase 3 o ~10.0 / 15.3 (W52) o ~-4.5 / -4.6 (W52) o JAK/TYK2 class; serious infections 10% vs 1% placebo ✓ Oral, once daily Efgartigimod FcRn antagonist · SC · Phase 3 o ~13.0 (Ph 2) / 14.8 (W24, Ph 2) nd ✓ AEs comparable to placebo o SC weekly (5mL) Anifrolumab Anti-IFNAR1 mAb · SC · Phase 3 nd nd o Broad IFN blockade; increased infection risk (viral reactivation) o SC weekly IVIG (Octagam 10%) Immunoglobulin · IV · Approved ✓ 24.9 / 26.8 (W16) o nd / -8.0 (W16) o Thrombotic/renal risk; infusion reactions IV 2 g/kg over 2–5 days, every 4 weeks
Page 42
JADE301 Phase 1 healthy volunteer study expected to begin Q4 2026; interim data anticipated in 2H 2027 Phase 1 Study Design Placebo-controlled, single ascending -dose study SC administration in healthy volunteers (N=24) Objectives PR IM A R Y ▪ Safety and tolerability S E CO ND A RY & E XP LO R AT O RY ▪ Pharmacokinetics ▪ Pharmacodynamics ▪ Immunogenicity Phase 1 HV study designed to generate key data supporting JADE301's potential for best- in-disease clinical activity and convenient SC dosing S C D OS E 1 : N = 6 : 2 S C D OS E 2 : N = 6 : 2 S C D OS E 3 : N = 6 : 2 Notes: Numbers presented as subjects receiving JADE301 relative to placebo. 42 JA DE301
Page 43
PR O GR A M MO A PR E CL I NI CA L PH A S E 1 PH A S E 2 PH A S E 3 PO T EN T IA L IN DI CA T IO NS JADE101 anti-APRIL IgAN JADE201 anti-BAFF-R Multiple systemic AI diseases JADE301 anti-IFN-β Dermatomyositis Advancing potentially best-in-class therapies for autoimmune diseases CO MPA NY OV ERV IEW Well-funded through multiple upcoming milestones; runway into the fourth quarter of 2028 Notes: Jade has entered into exclusive license agreements with Paragon Therapeutics for JADE101, JADE201 and JADE301. AI – Autoimmune; IgAN - IgA nephropathy; BAFF-R – B cell-Activating Factor Receptor; IFN-B – Interferon Beta; MoA – Mechanism of Action 43 Candidates designed to maximize clinical activity and allow patient friendly, infrequent dosing Development candidates from Paragon JA DE 101 ▪ Interim Phase 2 Data: 2027 ▪ Phase 3 Initiation: 1H 2027 JA DE 2 0 1 ▪ Interim Phase 1 Data: 2027 JA DE 301 ▪ Phase 1 Initiation: 4Q 2026 ▪ Interim Phase 1 Data: 2H 2027 Expected Milestones:
Page 44
Common stock Shares outstanding 63,556,065 Common stock equivalents Preferred stock (as converted to common stock) Pre-funded warrants 12,622,000 7,715,189 Common stock & common stock equivalents Total outstanding 83,893,254 Current capitalization Notes: As of June 30, 2026 44 CU RR ENT CA PI T AL I ZA TI O N
Page 45
Thank you J A D E B I O S C I E N C E S . C O M I N F O @ J A D E B I O S C I E N C E S . C O M N A S D A Q : J B I O