Bridgebio Pharma, Inc. · NASDAQ:BBIO
Bridgebio Pharma — Investor Presentation (January 2026)
83 slides from Bridgebio Pharma's investor presentation, Jan 12, 2026
Slide 1: Corporate Presentation
Corporate Presentation January 12, 2026
Slide 2: Forward Looking Statements and Disclaimer
Forward Looking Statements and Disclaimer The presentation contains forward-looking statements. Statements made or presented may include statements that are not historical facts and are considered forward-looking within the meaning of Section 27A of the Securities Act of 1933, as amended, and Sectio
Slide 3: BridgeBio's objective function
BridgeBio’s objective function Patient impact… …through sustainable value creation 𝑡𝑡 𝑁𝑁 ∆𝑄𝑄𝑄𝑄𝑄𝑄𝑄𝑄 (𝑖𝑖) Objective: max � � ∗ 𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝 (𝑖𝑖) Each program must be: 0 𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝𝑝 𝐷𝐷𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟 𝑖𝑖=1 • Based on beautiful science with a…
Slide 4: BridgeBio is a new type of biopharmaceutical company
BridgeBio is a new type of biopharmaceutical company From: To: Slow and bureaucratic decision making Rapid and decentralized decision making Expensive platforms with long lead times Assets selected to target genetic diseases before proof-of-concept data at their source High fixed costs Variablized a
Slide 5: The right approach: decentralized R&D, centralized infrastructure
The right approach: decentralized R&D, centralized infrastructure Build “minimum viable companies” to Build central infrastructure for de-risk programs as quickly and functions with economies of scale, efficiently as possible such as commercial Leverage hyper-experienced Leverage seasoned company R&
Slide 6: The right space: capitalizing on a scientific revolution to treat a massive unmet need
The right space: capitalizing on a scientific revolution to treat a massive unmet need for genetic diseases There are 10,000+ counted rare diseases affecting 450 million+ people globally ~3,000 without Genetics known molecular cause ~500 with approved Macromolecules therapies Clinical Diagnosis Ther
Slide 7: We have built a sustainable, high velocity engine to deliver hope and medicines
We have built a sustainable, high velocity engine to deliver hope and medicines to the patients that we serve > 8,500 patients impacted by our therapies Obtained Approval for 3 Medicines 2 Positive + 2 Ongoing Phase 3 Results Pivotal Trials 15 > 70 > 35 19 < $40M active trials papers academic IN
Slide 8: We leverage lean operating teams that advance medicines quickly and efficiently
We leverage lean operating teams that advance medicines quickly and efficiently for patients Topline BBP-418 IND ~5.5 Years for LGMD2I Topline IND ~6 Years Encaleret for ADH1 Topline IND ~6 Years Acoramidis for ATTR-CM Data on file. 7
Slide 9: We target well-described diseases at their source, underpinning industry-leading probability of technical success
We target well-described diseases at their source, underpinning our industry-leading probability of technical success Our approach Probability of Technical Success (POTS) 1. Characterize the genetic Clinical Dev. Industry BBIO source of the disease Stage Benchmark1 Historical2 Phase 1 52% 86% 2. Def
Slide 10: A pipeline of products that sing across the BridgeBio ecosystem
A pipeline of products that sing across the BridgeBio ecosystem Pre- Patients Market Program Indication Phase 1 Phase 2 Phase 3 Approved Clinical (US + EU) Opportunity Attruby Transthyretin Amyloidosis 500,000+ $20B+ (acoramidis) (ATTR-CM) Nulibry Molybdenum Cofactor Deficiency <100 Partnered (f
Slide 11: We are well-financed to hit a drumbeat of potential milestones in 2026 and beyond
NEW INFORMATION We are well-financed to hit a drumbeat of potential milestones in 2026 and beyond 1H 2026 Infigratinib: ACH Topline BridgeBio ended 2025 Encaleret: Initiate P2/3 pediatric ADH1 with $587.5M1 in cash, Encaleret: NDA filing cash equivalents, and marketable securities BBP-418: NDA filin
Slide 12: Attruby Approved for ATTR-CM
Attruby® Approved for ATTR-CM
Slide 13: Key Attruby highlights
Key Attruby highlights First and only approved product with a label specifying near-complete stabilization of TTR Effect seen as early as 1 month – reduction in cumulative cardiovascular outcomes within the first month of treatment in patients with ATTR-CM 42% reduction in composite of all-cause mor
Slide 14: $146M Q4 2025 Net Product Revenue
NEW INFORMATION Continued Attruby commercial momentum $146M 1 Q4 2025 Net Product Revenue 1Represents preliminary, unaudited results for the fourth quarter ended December 31, 2025, based on management’s current expectations and subject to completion of year end audit procedures. See Forward Looking
Slide 15: Continued commercial momentum and patient impact
NEW INFORMATION Continued commercial momentum and patient impact 6,629 1,632 >25% Unique U.S. patient Unique U.S. Estimated share of prescriptions for Attruby prescribing HCPs NBRx for Attruby As of December 31st, 2025 14
Slide 16: Our responsibility to patients spans beyond R&D
Our responsibility to patients spans beyond R&D – we are committed to ensuring the best access and affordability of any ATTR-CM medicine Dedicated patient support team Insurance navigation and support Ensuring easy and fast access: The least expensive ATTR treatment: Attruby can be delivered to a pa
Slide 17: We make it easy through simplified, differentiated, and generous access programs
We make it easy through simplified, differentiated, and generous access programs 28-day supply for patients new to Attruby Free Trial (newly diagnosed or switching from another therapy) Distribution Independent and rare/orphan disease–focused Specialty Pharmacies (SPs) Network where Institutional SP
Slide 18: Beyonttra has seen rapid EU uptake with leading guideline endorsements
Beyonttra® (acoramidis) has seen rapid EU uptake with leading guideline endorsements Beyonttra (acoramidis) Demonstrates Robust Commercial Global Guidelines Endorse Beyonttra (acoramidis) Uptake in Germany, Exceeding Projections for Clinical Confidence, Credibility, and Impact Achieved by Germany 7
Slide 19: ATTR is a multi-billion-dollar market primed for continued expansion
ATTR is a multi-billion-dollar market primed for continued expansion Global annual ATTR market sales1 $B $15-$202 $14 Market growth drivers include: $12 • With more sponsors, $10 $8.93 there is expanding +53% disease awareness $8 $2.2 $6.8 • Increased global $6 adoption of non- $4.3 $4 $3.2 invasive
Slide 20: Demand study shows significant Attruby market potential
Demand study shows significant Attruby market potential vs. partial stabilizer and partial knockdown Surveyed HCPs expect 30 - 40%+ peak market share for Attruby HCP sentiment towards Attruby is positive Attruby Market Share as % of Future Competitive Market Acoramidis showed dramatic reduction in (
Slide 21: We continue to research the differentiated clinical role of Attruby
NEW INFORMATION We continue to research the differentiated clinical role of Attruby 11 published manuscripts across 8 journals and 47 abstracts across 9 conferences in 2025 Clinical Outcomes Variant Biomarkers HEOR/Other 2026 Themes Prevention / Variant Arrhythmias Early Tx Effect Biomarkers And mor
Slide 22: Attruby significantly reduced the risk of CVM or recurrent CVH through Month 30
Attruby significantly reduced the risk of CVM or recurrent CVH through Month 30 vs. placebo by 49% with curve separation starting by Month 1 Estimated Mean Cumulative Events of CVM or Recurrent CVH Through Month 30 (mITT Population, Acoramidis, n = 409; Placebo, n = 202) Acoramidis Placebo (n = 409)
Slide 23: Published OLE data support Attruby's benefit on ACM and ACM/Recurrent CVH
Published data from the OLE further support Attruby’s statistically significant benefit on ACM and ACM/Recurrent CVH ACM1 ACM/Recurrent CVH2 M30 M36 M30 M36 0% -10% Relative Risk Reduction -20% -30% 25% -40% 36% -50% 42% 46% -60% Attruby resulted in a statistically significant ACM and ACM/Recurrent
Slide 24: Attruby delivers outstanding results in patients with poor prognosis
Attruby delivers outstanding results in patients with poor prognosis Natural History ATTRibute-CM mITT Population V122I ATTRv-CM has an aggressive Statistically significant benefit on composite ACM or phenotype and poor prognosis1 first CVH in ATTRv-CM participants vs. placebo2 Hazard Ratio 60 N (%)
Slide 25: Acoramidis reduced the risk of AF adverse events and AF-related hospitalizations
Acoramidis reduced the risk of AF adverse events and AF-related cardiovascular hospitalizations Incidence AF Adverse Event Annual Frequency of CVH Due to AF 30% RRR, 17% 0.035 RRR, 43% 0.03 Occurrence of atrial arrythmia event, % 25% to AF-related events per year, mean 25.1% 0.03 Annual frequency of
Slide 26: Additional data: Elevated TTR levels are associated with improved survival
Additional data: Elevated TTR levels are associated with improved survival Higher TTR concentration associated with Each 5 mg/dL rise in serum TTR is associated greater life expectancy (N≈102K individuals)1 with ~32% lower odds of death by 30 months Acoramidis Hazard ratio (95% CI) TTR distribution
Slide 27: Recruitment continues for ACT-EARLY, the first ATTR primary prevention trial
Recruitment continues for ACT-EARLY, the first ATTR primary prevention clinical trial, opening a new potential therapeutic paradigm for patients Current therapeutic paradigm: slow the progression of disease in patients with diagnosed ATTR 130+ ATTR Variants ~600 Participants ACT-EARLY is exploring w
Slide 28: BridgeBio has initiated a depleter program for ATTR-CM disease reversal
NEW PROGRAM BridgeBio has initiated a depleter program to explore the potential of ATTR-CM disease reversal ATTR-CM Disease Pathophysiology Led by Renowned Antibody Expert Existing TTR therapies target upstream …but unmet need remains for patients with existing tetramer stabilization and synthesis…
Slide 29: BridgeBio's depleter is engineered across 4 novel properties
NEW PROGRAM BridgeBio’s depleter is engineered across 4 novel properties for potential differentiation on clinical efficacy and dosing convenience Depleter Mechanism of Action BridgeBio’s Differentiated Target Properties 1 Improved fibril:tetramer binding ratio • >10× preferential binding to misfold
Slide 30: Limitations of first-generation depleters highlight next-generation opportunity
NEW PROGRAM Limitations of first-generation depleters highlight the opportunity for a next-generation depleter to better serve patient needs Competitors BridgeBio Property Company A Company B BridgeBio’s Depleter Why it Matters • Maximizes on-target Improved >10× preferential binding to engagement
Slide 31: BBP-418
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Slide 32: BBP-418 for LGMD2I/R9: thank you to patients and families
BBP-418 for Limb-Girdle Muscular Dystrophy Type 2I/R9 (LGMD2I/R9) A sincere THANK YOU to patients, families, advocates, investigators, clinical research staff, and collaborating research partners 31
Slide 33: LGMD2I/R9 is a progressive neuromuscular disease with high unmet need
LGMD2I/R9 is a progressive neuromuscular disease with high unmet need, representing a >$1B market opportunity in the US and EU Addressable patients by indication Unmet need • LGMD2I/R9 is an inherited neuromuscular disorder 9K characterized by lower-limb weakness and loss of ambulation as well as re
Slide 34: BBP-418 is an oral, disease-modifying therapy targeting LGMD2I/R9 at its source
BBP-418 is an oral, disease-modifying therapy that targets LGMD2I/R9 at its source by restoring glycosylation of alpha-dystroglycan Mechanism Design Principles FKRP glycosylates alpha-dystroglycan (αDG), stabilizing muscle cells by binding extracellular ligands to act as a “shock absorber” for mus
Slide 35: FORTIFY is an ongoing randomized, placebo-controlled Phase 3 study
FORTIFY is an ongoing randomized, placebo-controlled Phase 3 study; we reported topline results from a planned interim analysis in Oct. 2025 BBP-418 (N=74) BBP-418 (N~74) Screening Interim Analysis • Genetically (N=72) Randomization Open Label confirmed, 2:1 (N=112) Extension symptomatic Topline LGM
Slide 36: Interim analysis topline data reflect highly statistically significant results
Interim analysis topline data reflect highly statistically significant results on all pre-specified endpoints, including biomarker and clinical measures at 12 months BBP-418 in LGMD2I/R9: FORTIFY Phase 3 interim analysis topline results Primary endpoint (3 months) p-value Change from baseline in gly
Slide 37: Unprecedented and consistent improvement across primary and key secondary endpoints
Unprecedented and consistent improvement across primary and all key secondary efficacy endpoints combined with well-tolerated safety profile Ph. 3 FORTIFY interim analysis Type Endpoint Upside case target Outcome observed • Statistically significant increase vs. placebo Highly statistically signif
Slide 38: Significant increase in glycosylated αDG sustained at 12 months
Interim analysis showed statistically significant increase (+17% of control) from baseline in glycosylated αDG for BBP-418 treated, which was sustained at 12 months Change from baseline in glycosylated αDG (+/- 99% CI) 40 Glycosylated αDG (% of control) BBP-418 Placebo p<0.0001 LS Mean Estimate CFB
Slide 39: Large, statistically significant reduction in serum CK
In addition, BBP-418 treated patients experienced a large, statistically significant reduction in serum CK of 82% from baseline at 12 months Reduction in muscle damage Change from baseline in serum creatine kinase (U/L) 400 186 0 -400 -800 -1,869 -1,200 -1,600 -2,000 Placebo BBP-418 (n=22) p<0.0001
Slide 40: Difference of 0.27 m/s in 100MTT versus placebo
Results translated to clinical endpoints with a difference of 0.27 m/s between BBP-418 and placebo in 100MTT, translating to a difference of ~14 seconds faster Improved ambulatory function Change from baseline in 100-meter timed test (m/s) 0.15 0.10 0.14 0.05 0.00 -0.05 -0.12 -0.10 -0.15 Placebo BBP
Slide 41: BBP-418 improved FVC versus placebo
BBP-418 treated individuals also registered ~3% increase in predicted volume from baseline FVC, resulting in a difference of ~5% predicted volume vs. placebo Improved pulmonary function Change from baseline in forced vital capacity, sitting position (% predicted) 3 2 3.0% 1 ~2% decline is consistent
Slide 42: Clinically meaningful 2.6 point benefit on NSAD
NEW INFORMATION In an exploratory analysis, BBP-418 treated patients experienced highly clinically meaningful 2.6 point benefit on NSAD relative to placebo even at early 12-month timepoint Improved gross motor function Even a 1-point difference in NSAD can mean… Change from baseline in NSAD (points)
Slide 43: More than stabilization: improvements across clinical endpoints at 12 months
NEW INFORMATION More than stabilization: BBP-418 treated individuals experienced meaningful improvements across clinical endpoints at 12 months Improved ambulatory function Improved pulmonary function Improved gross motor function CFB in 100MTT (m/s) CFB in FVC (% predicted) CFB in NSAD (points) 0.1
Slide 44: Planned subgroup analyses show consistent benefit
NEW INFORMATION Planned subgroup analyses show consistent benefit of BBP-418 vs. placebo in all subgroups across α-controlled endpoints at 12 months Biomarker Glycosylated αDG (% of control) Serum creatine kinase (U/L) LS Mean Difference (95% CI) LS Mean Difference (95% CI) L276I homozygous L276I ho
Slide 45: Interim analysis reflects highly favorable safety profile of BBP-418
Interim analysis results continue to reflect highly favorable safety profile of BBP-418 • No new or unexpected safety findings have been observed; results consistent with Ph. 2 • Discontinuation rate was low overall and higher in the placebo group • No treatment-related serious TEAEs were observed I
Slide 46: Successful FDA meeting post interim analysis; NDA toward traditional approval
NEW INFORMATION We completed a successful meeting with FDA post interim analysis, and they recommend orienting our NDA toward traditional approval Positive topline Oct. 2025 File New 1H 2026 results from Phase Drug 3 FORTIFY study Application interim analysis (NDA) with FDA U.S. Approval and Comme
Slide 47: Encaleret
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Slide 48: Encaleret for ADH1: thank you to patients and families
encaleret for Autosomal Dominant Hypocalcemia Type 1 (ADH1) A sincere THANK YOU to the patients, families, advocates, investigators, clinical research staff, referring providers, and collaborating research partners 47
Slide 49: No therapies currently indicated to treat ADH1
There are no therapies currently indicated to treat ADH1, a serious and rare genetic condition An analogous ADH1 market is XLH 12K Individuals with ADH1 XLH ADH1 ~12K ADH1 prevalent Prevalence (US) 12K5 12K population in the US based on Acute - hypocalcemia Disease burden Hypophosphatemia 4 populati
Slide 50: Encaleret targets the underlying disease mechanism of ADH1
Encaleret is an investigational, potential first-in-class therapy that targets the underlying disease mechanism of ADH1 Design Principles Only investigational treatment directly targeting ADH1 at its source Potential to restore physiologic mineral homeostasis that is disrupted by CaSR oversensitivit
Slide 51: HCPs report low satisfaction with conventional therapy
NEW INFORMATION Endocrinologists & nephrologists report low satisfaction with conventional therapy, leading to strong interest in novel investigational agents like HCPs encaleret are not satisfied with conventional therapy High likelihood HCPs would prescribe encaleret Dissatisfaction with Currently
Slide 52: Encaleret Phase 3 registrational study design
Encaleret phase 3 registrational study design Screening and SOC Encaleret Encaleret Titration Period (N=45) Maintenance Optimization Period Period • Age > 16 years of age • Documented pathogenic, Participants randomized to encaleret stopped SoC prior to first dose Long-Term Extension likely pathogen
Slide 53: >90% of CALIBRATE participants demonstrated a pharmacologic response
>90% of CALIBRATE participants administered encaleret demonstrated a pharmacologic response Week 4 Week 24 Primary Analysis – Within Group SoC Encaleret p-value3 (N=45) (N=45) Number of Participants Meeting The Primary Endpoint 2 34 (Responder status)1,2 Proportion, % 4% 76% Difference in Proportion
Slide 54: Encaleret was well-tolerated with no TEAEs resulting in discontinuation
Encaleret was well-tolerated with no TEAEs resulting in encaleret or study discontinuation Period 1 Periods 2 and 3 SoC SoC Encaleret N=67 N=22 N=45 Participants experiencing any Serious TEAE 2 (3%) 3 (14%) 4 (9%) Serious Related TEAE 1 (2%) 0 (0%) 1 (2%) Participants experiencing any TEAE 30 (45%)
Slide 55: Encaleret restored physiologic mineral homeostasis through CaSR
Encaleret was found to restore physiologic mineral homeostasis through its action on the CaSR • 76% of participants randomized to encaleret achieved serum and urine calcium in the target range compared to the same individuals on conventional therapy (difference 71%, p<0.0001)1,2 • Among encaleret re
Slide 56: CALIBRATE achieved and exceeded all upside target criteria
CALIBRATE achieved & exceeded all criteria set forth as an upside target, with a 76% responder rate following 24 weeks of encaleret treatment Upside Target Clinical Profile Outcome Observed Statistically significant primary analysis result Primary endpoint met (p <0.0001) demonstrating compared to
Slide 57: Pioneering efforts to enable the successful launch of encaleret
BridgeBio is pioneering efforts to enable the successful launch of NEW INFORMATION encaleret, potentially the first calcilytic molecule to be approved for any condition Expanded availability of testing Enabled creation of new Enabled update to treatment through sponsored genetic ICD-10 code dedicate
Slide 58: Over 24 months, >1,700 unique patients diagnosed with ADH in the US
Over a 24-month period, >1,700 unique patients were diagnosed NEW INFORMATION with ADH in the US Cumulative ADH Patients Diagnosed2 1,800 1,600 1,400 1,200 17% CMGR 1,000 800 600 400 200 0 10/23 01/24 04/24 07/24 10/24 01/25 04/25 07/25 10/25 ~50% of HCPs diagnosing ADH patients manage ≥5 non-surgic
Slide 59: Encaleret potential as oral medication for other etiologies of chronic hypoparathyroidism
Encaleret also has potential as an oral medication for other etiologies of chronic hypoparathyroidism (HP) Encaleret expansion Chronic Hypoparathyroidism opportunity (~200K in US+EU)1,2,3 (RECLAIM-HP trial) Post-surgical Genetic Autoimmune Idiopathic (65%-75%)4,5 (~12.5%)5 (<10%)5 (<10%)5 Encaleret
Slide 60: Normalization of calcium homeostasis in post-surgical hypoparathyroidism patients
Normalization of calcium homeostasis in post-surgical hypoparathyroidism (PSH) patients is indicative of encaleret’s broader potential Effect on PTH in PSH patients1,2 Effect on calcium homeostasis in PSH patients1,2 (N = 10) (N = 10) Fractional Excretion of Calcium Parathyroid Hormone (pg/mL) Corre
Slide 61: Encaleret potential as oral option for chronic hypoparathyroidism
NEW INFORMATION Encaleret has the potential to be an orally administered option for patients with chronic hypoparathyroidism (CHP) Announcing the RECLAIM-HP Encaleret has the potential to normalize Phase 3 Study of Encaleret in CHP blood and urine calcium in CHP patients Initiating in 2026 • CHP pat
Slide 62: RECLAIM-HP Phase 3 study to initiate in Summer 2026
NEW INFORMATION RECLAIM-HP Phase 3 study of encaleret in chronic hypoparathyroidism to initiate in Summer 2026 RECLAIM-HP: Global, multi-center, randomized, double-blind, placebo-controlled study Double-blinded treatment period Encaleret + Conventional Therapy1 Encaleret + Conventional Therapy1 Titr
Slide 63: NDA submission for ADH1 planned in first half of 2026
NDA submission for ADH1 planned in the first half of 2026 with two additional registrational studies planned for initiation next year Positive topline Oct. 2025 Initiate Phase 2/3 Submit New Drug 1H 2026 Q1 2026 results from study in Pediatric Application (NDA) Phase 3 CALIBRATE ADH1 to FDA regist
Slide 64: Infigratinib
Infigratinib
Slide 65: Significant unmet need for children with skeletal dysplasias
There remains a significant unmet need for many children with skeletal dysplasias; this represents a large and rapidly growing market Addressable people by indication in US/EU1 (current population eligible for treatment) 55,000 Represents 15-25K individuals with diagnosed and addressable ACH 1.5-2.5
Slide 66: Infigratinib is a potentially best-in-class FGFR3 inhibitor
Infigratinib is a potentially best-in-class FGFR3 inhibitor that targets achondroplasia and hypochondroplasia at their source Mechanism Design Principles FGFR3 FGFR3 Gain-of-function Maximize efficacy by targeting variant condition at the source Infigratinib For all the manifestations of ACH and HCH
Slide 67: At 18 months, infigratinib shows persistent improvement in AHV and body segmentation
At 18 months, infigratinib has shown persistent improvement in AHV and body segmentation, along with a favorable safety profile Mean change from baseline in annualized height velocity Upper body to lower body segment ratio (AHV) (Lower value means improved proportionality) +3.38 cm/yr 2.05 +2.51 cm/
Slide 68: Fully enrolled Phase 3 study (PROPEL 3) in achondroplasia
We have fully enrolled a Phase 3 study (PROPEL 3) of infigratinib in Achondroplasia and expect topline results in early 2026 0.25 mg/kg/day Infigratinib (N ~ 76) Open Label Screening and Extension Observational Period Randomization Children are Children are followed 2:1 followed until for a minimum
Slide 69: LPLV achieved on PROPEL 3; topline expected Q1
NEW INFORMATION We have achieved LPLV on PROPEL 3 and expect topline in Q1, and we have made significant operational progress on expansion opportunities Last participant last visit completed; Topline expected Q1 2026 Pivotal Phase 3 Study in children and adolescents (3-<18 years) with achondroplasia
Slide 70: Defining characteristics of a potentially best-in-class program in ACH
Infigratinib: Defining characteristics of a potentially best-in-class program in the ACH landscape Designed to target achondroplasia at its genetic source: FGFR3 overactivation Addresses not just overactivation of the MAPK pathway (chondrocyte hypertrophy), but also STAT1 (chondrocyte proliferation)
Slide 71: Infigratinib sprinkle capsules are being developed for oral administration
Infigratinib sprinkle capsules are being developed for oral administration 1,2 • Infigratinib is being studied in children over 3 years of age with achondroplasia Capsules (17 mm long*) Granules (2 mm long) (0.25 kg/mg/day) as a sprinkle capsule • Capsules can be swallowed whole or content (granules
Slide 72: Validated evidence-based perspective to forecasting market share performance
BridgeBio has developed a validated evidence-based perspective to forecasting market share performance Comprehensive market surveys Analog research shows 2nd entrants ML-based empirical analysis enables indicated 30-40%+ Attruby share achieve average ~37% share high fidelity drug launch modeling Att
Slide 73: Infigratinib could capture >50% of treated market share
Our market research indicates that infigratinib could capture >50% of treated market share, primarily driven by the favorable oral administration and MOA Potential share for ACH children Attribute TPP for testing market share % of treated children • Children (3 – 18 years) with (N = 95 HCPs; represe
Slide 74: Hypochondroplasia is a FGFR3-related skeletal dysplasia
Hypochondroplasia is a FGFR3-related skeletal dysplasia • Autosomal dominant condition Infigratinib directly targets FGFR3 signaling • Similar incidence to achondroplasia • Greater genetic heterogeneity in FGFR3 pathogenic variants (e.g. N540K in addition to others) • Clinical features: • Moderate d
Slide 75: Hypochondroplasia is a large, mechanistically de-risked expansion opportunity
Hypochondroplasia is a large, mechanistically de-risked expansion opportunity; First participant dosed in Phase 2 study Rationale for infigratinib Recent progress and upcoming milestones Directly targets the underlying cause of hypochondroplasia, FGFR3 overactivity1,2 Observational run-in study for
Slide 76: BBP-812
BBP-812
Slide 77: Canavan disease is a severe, fatal, ultra-rare pediatric disease
Canavan disease is a severe, fatal, and ultra-rare neurodegenerative pediatric disease with no approved therapies Unmet need • Canavan disease (CD) is an ultra-rare neurodegenerative disease with ~1,000 patients across the US and EU • CD is usually fatal within the first two decades of life, and >25
Slide 78: BBP-812 is a potentially first-in-class, disease-modifying therapy
BBP-812 is a potentially first-in-class, disease-modifying therapy that targets Canavan disease directly at its source Mechanism Design Principles Provide first disease-modifying therapy Target the condition directly at the source, utilize single registrational study & biomarker for accelerated appr
Slide 79: Current path to a potential BLA filing based on urine NAA reductions
NEW INFORMATION Current path to a potential BLA filling in 2027 based on reductions in urine NAA (surrogate endpoint) supported by motor function improvements Urine N-acetylaspartic acid (NAA) levels Hammersmith Infant Neurological Examination (HINE-2) Trajectory Change in HINE-2 Total Score Months
Slide 80: BridgeBio Ecosystem Highlights
BridgeBio Ecosystem Highlights
Slide 81: BBOT has progressed a pipeline of molecules into the clinic
NEW INFORMATION BBOT has progressed a pipeline of molecules into the clinic that are poised to close key activity gaps in the RAS-focused therapeutic space BBO-8520 BBO-11818 BBO-10203 First direct inhibitor Potent, direct inhibitor Novel RAS:PI3Kα Breaker of KRASG12C ON/OFF with of panKRAS ON/OFF s
Slide 82: The GondolaBio pipeline features a diverse set of programs
NEW INFORMATION The GondolaBio pipeline features a diverse set of programs across therapeutic areas and modalities Patient Population IND Indication Discovery Lead Op Phase 1 Phase 2 (US+EU) Enabling Erythropoietic Protoporphyria (EPP) 25k Autosomal Dominant Polycystic Kidney Disease (ADPKD) 300k Al
Slide 83: About Attruby and BridgeBio
About Attruby® (acoramidis) Attruby is the only near-complete (≥90%) stabilizer of Transthyretin (TTR) approved in the U.S. for the treatment of adult patients with ATTR-CM to reduce cardiovascular death and cardiovascular-related hospitalization. Attruby was generally well-tolerated. The most commo
BridgeBio Pharma — Investor Presentation (January 2026) on 6ix