Exhibit 99.1 Nasdaq: CBIO HARNESSING THE CATALYTIC POWER OF PROTEASES Complement R&D Day 19 July 2021 CatalystBiosciences.comExhibit 99.1 Nasdaq: CBIO HARNESSING THE CATALYTIC POWER OF PROTEASES Complement R&D Day 19 July 2021 CatalystBiosciences.com
Forward-looking statements Certain information contained in this presentation and statements made orally during this presentation include forward-looking statements that involve substantial risks and uncertainties. All statements included in this presentation, other than statements of historical facts, are forward looking statements. Forward-looking statements include, without limitation, statements about the product candidates of Catalyst Biosciences, Inc. (the “Company”) and the benefits of its protease engineering platform; the potential markets for and advantages of the Company's complement product candidates, including CB 2782-PEG, CB 4332 and complement degraders; plans for the Company's collaboration with Biogen; and plans to enroll the CB 4332 observational trial in mid-2021 and to conduct human clinical trials and report pK and biomarker data for CB 4332 in 2022. Actual results or events could differ materially from the plans, intentions, expectations and projections disclosed in the forward-looking statements. Various important factors could cause actual results or events to differ materially, including, but not limited to, the risk that trials and studies may be delayed as a result of COVID-19 and other factors, that trials may not have satisfactory outcomes, the risk that costs required to develop or manufacture the Company’s products will be higher than anticipated, including as a result of delays in development and manufacturing resulting from COVID-19 and other factors, the risk that Biogen will terminate its agreement with the Company, competition and other risks described in the “Risk Factors” section of the Company’s Annual Report on Form 10-K filed with the Securities and Exchange Commission ( SEC ) on March 4, 2021, on Form 10-Q filed with the SEC on May 6, 2021, and in other filings with the SEC. The forward-looking statements in this presentation represent the Company's view as of the date of this presentation and the Company does not assume any obligation to update any forward-looking statements, except as required by law. 2Forward-looking statements Certain information contained in this presentation and statements made orally during this presentation include forward-looking statements that involve substantial risks and uncertainties. All statements included in this presentation, other than statements of historical facts, are forward looking statements. Forward-looking statements include, without limitation, statements about the product candidates of Catalyst Biosciences, Inc. (the “Company”) and the benefits of its protease engineering platform; the potential markets for and advantages of the Company's complement product candidates, including CB 2782-PEG, CB 4332 and complement degraders; plans for the Company's collaboration with Biogen; and plans to enroll the CB 4332 observational trial in mid-2021 and to conduct human clinical trials and report pK and biomarker data for CB 4332 in 2022. Actual results or events could differ materially from the plans, intentions, expectations and projections disclosed in the forward-looking statements. Various important factors could cause actual results or events to differ materially, including, but not limited to, the risk that trials and studies may be delayed as a result of COVID-19 and other factors, that trials may not have satisfactory outcomes, the risk that costs required to develop or manufacture the Company’s products will be higher than anticipated, including as a result of delays in development and manufacturing resulting from COVID-19 and other factors, the risk that Biogen will terminate its agreement with the Company, competition and other risks described in the “Risk Factors” section of the Company’s Annual Report on Form 10-K filed with the Securities and Exchange Commission ( SEC ) on March 4, 2021, on Form 10-Q filed with the SEC on May 6, 2021, and in other filings with the SEC. The forward-looking statements in this presentation represent the Company's view as of the date of this presentation and the Company does not assume any obligation to update any forward-looking statements, except as required by law. 2
Welcome Catalyst Biosciences: The Protease Medicines Company Nassim Usman, Ph.D. | President & CEO
Complement R&D Day – July 2021 Agenda Time Topic (Speaker) 12:00 - 12:05 pm Catalyst Biosciences: The Protease Medicines Company Nassim Usman, Ph.D. | Catalyst President & CEO 12:05 - 12:25 pm The Need for Complement Factor I Replacement Filomeen Haerynck, M.D., Ph.D. | KOL, Ghent University 12:25 - 12:45 pm Growing Complement Pathway Protease Platform Grant Blouse, Ph.D. | Catalyst CSO 12:45 - 12:50 pm Milestones Clinton Musil | Catalyst CFO 12:50 - 1:10 pm Q&A Session 4Complement R&D Day – July 2021 Agenda Time Topic (Speaker) 12:00 - 12:05 pm Catalyst Biosciences: The Protease Medicines Company Nassim Usman, Ph.D. | Catalyst President & CEO 12:05 - 12:25 pm The Need for Complement Factor I Replacement Filomeen Haerynck, M.D., Ph.D. | KOL, Ghent University 12:25 - 12:45 pm Growing Complement Pathway Protease Platform Grant Blouse, Ph.D. | Catalyst CSO 12:45 - 12:50 pm Milestones Clinton Musil | Catalyst CFO 12:50 - 1:10 pm Q&A Session 4
The Protease Medicines Company Harnessing the catalytic power of proteases Novel differentiated medicines Robust complement portfolio Clinical-stage assets Unique expertise in protease engineering 5The Protease Medicines Company Harnessing the catalytic power of proteases Novel differentiated medicines Robust complement portfolio Clinical-stage assets Unique expertise in protease engineering 5
Catalyst protease platform Unique expertise enables design of optimized & differentiated protease candidates Discovery Platform Our Proteases + Functionally enhance Protease Protease natural proteases in Scaffold Candidate the complement & coagulation cascades + Engineer novel protein degraders in the complement cascade + Modulate or target biological activation or inactivation Structure Guided Design Engineered Regulation Molecular Evolution Pharmacokinetic Improvement 6Catalyst protease platform Unique expertise enables design of optimized & differentiated protease candidates Discovery Platform Our Proteases + Functionally enhance Protease Protease natural proteases in Scaffold Candidate the complement & coagulation cascades + Engineer novel protein degraders in the complement cascade + Modulate or target biological activation or inactivation Structure Guided Design Engineered Regulation Molecular Evolution Pharmacokinetic Improvement 6
CB 2782-PEG (nM) Catalyst protease platform Validated across three programs Marzeptacog alfa Dalcinonacog alfa CB 2782-PEG (activated) 90% reduction Achieved sustained Best-in-class profile for dry AMD in annualized bleed rate & high target levels of FIX Extended pharmacodynamics 6 10000 Normal clotting levels 5 1000 4 100 50% 3 Mild Hemophilia 10 2 5% 1 1 Moderate Hemophilia 1% 0 0.1 Severe Hemophilia 0 10 20 30 40 50 Before treatment On treatment Days Engineered Engineered Novel rFVIIa protease rFIX protease C3 degrader 7 C3 Concentration (nM)CB 2782-PEG (nM) Catalyst protease platform Validated across three programs Marzeptacog alfa Dalcinonacog alfa CB 2782-PEG (activated) 90% reduction Achieved sustained Best-in-class profile for dry AMD in annualized bleed rate & high target levels of FIX Extended pharmacodynamics 6 10000 Normal clotting levels 5 1000 4 100 50% 3 Mild Hemophilia 10 2 5% 1 1 Moderate Hemophilia 1% 0 0.1 Severe Hemophilia 0 10 20 30 40 50 Before treatment On treatment Days Engineered Engineered Novel rFVIIa protease rFIX protease C3 degrader 7 C3 Concentration (nM)
Growing Complement Pathway Protease Platform Grant E. Blouse, Ph.D. | Chief Scientific OfficerGrowing Complement Pathway Protease Platform Grant E. Blouse, Ph.D. | Chief Scientific Officer
Proteases are ideal for high abundancy targets & cascades A better way to regulate biological processes compared with antibodies & small molecules Therapeutic target neutralization Protease Efficient regulation at low concentrations of therapeutic protease Antibodies Requires high concentrations in excess of the target Small molecules / peptides Requires high concentrations & frequent dosing 9Proteases are ideal for high abundancy targets & cascades A better way to regulate biological processes compared with antibodies & small molecules Therapeutic target neutralization Protease Efficient regulation at low concentrations of therapeutic protease Antibodies Requires high concentrations in excess of the target Small molecules / peptides Requires high concentrations & frequent dosing 9
Multiple, high-value complement programs Future Degraders NextGen Degraders Our Lead Candidate Novel Engineered Degrader Partnered with Biogen C3a C4b CB 2782-PEG CB 4332 C3b C5a Established Catalyst Biosciences in complement Leads expansion into systemic complement in CFI Specific & potent degraders dysregulation target classical & alternative Broadens Catalyst complement disorders with Biosciences footprint in large-market potential the complement space 10Multiple, high-value complement programs Future Degraders NextGen Degraders Our Lead Candidate Novel Engineered Degrader Partnered with Biogen C3a C4b CB 2782-PEG CB 4332 C3b C5a Established Catalyst Biosciences in complement Leads expansion into systemic complement in CFI Specific & potent degraders dysregulation target classical & alternative Broadens Catalyst complement disorders with Biosciences footprint in large-market potential the complement space 10
Unique targeted approach to complement regulation Cascade initiation Cascade regulation Terminal complement C4b Degraders NextGen Degraders CB 2782-PEG C3b Degraders Other programs CB 4332 C2 C1r Classical C4b C3a pathway C1s C4 Immune response inflammation Lectin C3b C3 C5a C5 MASP pathway C3 Alternative C3b FB C5b FD (H O) pathway 2 Membrane attack complex (MAC) 11Unique targeted approach to complement regulation Cascade initiation Cascade regulation Terminal complement C4b Degraders NextGen Degraders CB 2782-PEG C3b Degraders Other programs CB 4332 C2 C1r Classical C4b C3a pathway C1s C4 Immune response inflammation Lectin C3b C3 C5a C5 MASP pathway C3 Alternative C3b FB C5b FD (H O) pathway 2 Membrane attack complex (MAC) 11
CB 2782-PEG Novel engineered C3 degrader in complement 12CB 2782-PEG Novel engineered C3 degrader in complement 12
CB 2782-PEG: Long acting anti-C3 protease for dry AMD Geographic atrophy is a Best-in-class C3 Biogen collaboration high unmet need degrader for dry AMD + Advanced stage of dry age- + Generated from Catalyst’s + $15M upfront, up to $340M in related macular degeneration proprietary protease milestones & tiered royalties (dAMD) engineering platform up to low double digits + dAMD affects ~1M people in the + Potent, selective & long + Catalyst: fully funded pre- US & >5M WW, no currently acting, degrades C3 into clinical & manufacturing approved therapy inactive fragments activities + Global market ~ >$5B + NHP PK & PD data* predict + Biogen: IND-enabling best-in-class human activities, WW clinical intravitreal dosing 3 or 4 development & + C3 is a clinically validated target times a year commercialization (randomized P2) for dAMD *Furfine et al. ARVO 2019 13
CB 2782-PEG (nM) CB 2782-PEG (nM) CB 2782-PEG: Best-in-class C3 degrader for dry AMD Protease advantage demonstrated in vivo CB 2782-PEG degrades C3 levels in the eye for at Catalytic advantage of proteases least 28 days in a non-human primate model + One therapeutic molecule 6 10000 neutralizes 1000s 5 1000 + Fast & potent response 4 + Extended pharmacodynamic effect 100 3 + Can activate or degrade 10 therapeutic targets 2 + Engineered novel protein 1 1 degraders “sweep away” difficult to drug targets 0 0.1 0 10 20 30 40 50 Days Days 14 C3 Concentration (nM) C3 Concentration (nM)CB 2782-PEG (nM) CB 2782-PEG (nM) CB 2782-PEG: Best-in-class C3 degrader for dry AMD Protease advantage demonstrated in vivo CB 2782-PEG degrades C3 levels in the eye for at Catalytic advantage of proteases least 28 days in a non-human primate model + One therapeutic molecule 6 10000 neutralizes 1000s 5 1000 + Fast & potent response 4 + Extended pharmacodynamic effect 100 3 + Can activate or degrade 10 therapeutic targets 2 + Engineered novel protein 1 1 degraders “sweep away” difficult to drug targets 0 0.1 0 10 20 30 40 50 Days Days 14 C3 Concentration (nM) C3 Concentration (nM)
CB 2782-PEG: Comparison to APL-2 & NGM621 Potential for a less frequent dosing regimen in dry AMD APL-2 (Apellis) NGM621 (NGM Bio) CB 2782-PEG Category PEGylated cyclic peptide Antibody anti-C3 Protease Targets C3 Yes Yes Yes Dose Frequency Every 1-2 months Every 1-2 months Every ~3 months* Half-life in Cyno VH 3.2 days n/a 4.1 days Dose level 15 mg (high) 15 mg (none) up to 1 mg (low) (risk of PEG overload) 15 *Frequency estimated based on ocular PK-PD data in non-human primatesCB 2782-PEG: Comparison to APL-2 & NGM621 Potential for a less frequent dosing regimen in dry AMD APL-2 (Apellis) NGM621 (NGM Bio) CB 2782-PEG Category PEGylated cyclic peptide Antibody anti-C3 Protease Targets C3 Yes Yes Yes Dose Frequency Every 1-2 months Every 1-2 months Every ~3 months* Half-life in Cyno VH 3.2 days n/a 4.1 days Dose level 15 mg (high) 15 mg (none) up to 1 mg (low) (risk of PEG overload) 15 *Frequency estimated based on ocular PK-PD data in non-human primates
CB 4332: Enhanced Complement Factor I Next clinical candidate 16
Complement Factor I CFI is a key down-regulator of the complement cascade Applying the brakes to complement Classical Lectin Alternate pathway pathway pathway CFI is a key regulator of complement MBL C3(H O) C1q 2 activation targeting both C3b & C4b C1r • Classical & lectin pathway inhibitor MASPs CFD CFB C1s • Alternative pathway inhibitor C4 C2 CFI deficiency triggers uncontrolled pathway activation C3b Bb C4b 2b • Secondary complement deficiency C3 • Significant C3 depletion CFI • Susceptibility to infections & increased autoimmune complex diseases 17Complement Factor I CFI is a key down-regulator of the complement cascade Applying the brakes to complement Classical Lectin Alternate pathway pathway pathway CFI is a key regulator of complement MBL C3(H O) C1q 2 activation targeting both C3b & C4b C1r • Classical & lectin pathway inhibitor MASPs CFD CFB C1s • Alternative pathway inhibitor C4 C2 CFI deficiency triggers uncontrolled pathway activation C3b Bb C4b 2b • Secondary complement deficiency C3 • Significant C3 depletion CFI • Susceptibility to infections & increased autoimmune complex diseases 17
CB 4332: SQ Enhanced Complement Factor I Development candidate to restore regulation Rationale & unmet need + Rebalance the complement system in patients with dysregulated CFI + No specific therapies exist to correct CFI dysregulation + Targets population with no + Engineered for an extended half-life treatment or who respond + Once weekly SQ therapy – no PEG 1,2 poorly to current treatments + In vitro & Ex vivo activity comparable to native CFI + Classical & alternative pathway regulation + High yield production process 1 2 References: Bienaime et al. Kidney Int. 2010; Ferreira et al. Nefrologia. 2016; Note: CFH = Complement factor H; Structural model based on PDB 2XRC. 18CB 4332: SQ Enhanced Complement Factor I Development candidate to restore regulation Rationale & unmet need + Rebalance the complement system in patients with dysregulated CFI + No specific therapies exist to correct CFI dysregulation + Targets population with no + Engineered for an extended half-life treatment or who respond + Once weekly SQ therapy – no PEG 1,2 poorly to current treatments + In vitro & Ex vivo activity comparable to native CFI + Classical & alternative pathway regulation + High yield production process 1 2 References: Bienaime et al. Kidney Int. 2010; Ferreira et al. Nefrologia. 2016; Note: CFH = Complement factor H; Structural model based on PDB 2XRC. 18
CB 4332: To address CFI deficiency at the root cause Designed to provide unique advantages CB 4332 Unmet needs in CFI deficiency Designed to address Blocks complement-initiated cell destruction in the circulation Directly addresses root cause of disease Addresses extravascular hemolysis Preserves normal immune functions, e.g. to fight off infections Convenient weekly SQ administration 19CB 4332: To address CFI deficiency at the root cause Designed to provide unique advantages CB 4332 Unmet needs in CFI deficiency Designed to address Blocks complement-initiated cell destruction in the circulation Directly addresses root cause of disease Addresses extravascular hemolysis Preserves normal immune functions, e.g. to fight off infections Convenient weekly SQ administration 19
Screening & natural history of disease studies ConFIrm & ConFIdence: preparing for Phase 1/2 Identifies Target Population / Feeds ConFIdence Study / Discovers Undiagnosed Disease The ConFIrm Study CB CB 4 43 33 32 2 CB 4332 Ph Pha ase se 1 1//2 2 Phase 1/2 Tr Triia alls s Trials Sc Scr re ee en niin ng g The ConFIdence Study Prospective Clinical & Biomarkers Assessment of CFI-Deficiency Disease While on SoC Identification of CFI-deficient patients & key investigators for CB 4332 trials Discover undiagnosed disease, create program awareness & inform on biomarkers 20Screening & natural history of disease studies ConFIrm & ConFIdence: preparing for Phase 1/2 Identifies Target Population / Feeds ConFIdence Study / Discovers Undiagnosed Disease The ConFIrm Study CB CB 4 43 33 32 2 CB 4332 Ph Pha ase se 1 1//2 2 Phase 1/2 Tr Triia alls s Trials Sc Scr re ee en niin ng g The ConFIdence Study Prospective Clinical & Biomarkers Assessment of CFI-Deficiency Disease While on SoC Identification of CFI-deficient patients & key investigators for CB 4332 trials Discover undiagnosed disease, create program awareness & inform on biomarkers 20
CB 4332: Phase 1/2 - First in human study Study parts Study design + Phase 1 open-label, single & multiple ascending SQ doses & extended duration proof of concept Single Ascending Doses + Population: CFI-deficient patients (N=up to 12) Proposed starting dose + 0.5 mg/Kg Multiple Ascending Doses (N=up to 9) Goals + Safety & tolerability + PK characterization Extended treatment to assess + Assessment of complement biomarkers (C3, FB, FBb, proof of concept Bb/FB ratio, iC3b, C3d, C3dg, AP50/AH50) (N=up to 15) + Establish a Recommended Dose Regimen within the CFI normal range 21CB 4332: Phase 1/2 - First in human study Study parts Study design + Phase 1 open-label, single & multiple ascending SQ doses & extended duration proof of concept Single Ascending Doses + Population: CFI-deficient patients (N=up to 12) Proposed starting dose + 0.5 mg/Kg Multiple Ascending Doses (N=up to 9) Goals + Safety & tolerability + PK characterization Extended treatment to assess + Assessment of complement biomarkers (C3, FB, FBb, proof of concept Bb/FB ratio, iC3b, C3d, C3dg, AP50/AH50) (N=up to 15) + Establish a Recommended Dose Regimen within the CFI normal range 21
Diseases with CFI mutations have tremendous potential CFI Deficiency US / EU5 market opportunity Current development CFI Deficiency targets Recurrent Chronic First indication infections inflammation C3G aHUS IC-MPGN IC-MPGN $500M+ Market opportunity in C3G Geographic atrophy CFI deficient populations Potential aHUS targets Specific systemic therapies in development Autoimmune 0 for patients with dysregulated CFI disorders Therapies addressing the root cause of disease 0 Approved treatments for C3G, IC-MPGN, CFID 0 Note: aHUS = atypical Hemolytic Uremic Syndrome, C3G = Complement 3 Glomerulopathy, IC-MPGN = Immune-Complex Membranoproliferative Glomerulonephritis, CFID = Complement Factor I Deficiency References: Bresin et al. JASN. 2013; Fremeaux-Bacchi et al. ASN. 2013; Rui-Ru et al. Jour Rare Dis Res. 2018; Servais et al. Kidney Int. 2012; Iatropoulous et al. Mol Immunol. 2016; Hou et al. Kidney Int. 2014; Alba-Domiguez et al. J rare Dis. 2012. El Sissy et al. Front. Immunol. 2019; Shields et al. Front Immunol. 2019; Naesens et al. Jour Allergy & Clin Immunol. 2020. Yan et al. Clin Epi 2020; Smith et al. 22 Nature Reviews. 2019; Noris et al. Clin J Am Soc Nephrol. 2010; CBIO KOL interviewsDiseases with CFI mutations have tremendous potential CFI Deficiency US / EU5 market opportunity Current development CFI Deficiency targets Recurrent Chronic First indication infections inflammation C3G aHUS IC-MPGN IC-MPGN $500M+ Market opportunity in C3G Geographic atrophy CFI deficient populations Potential aHUS targets Specific systemic therapies in development Autoimmune 0 for patients with dysregulated CFI disorders Therapies addressing the root cause of disease 0 Approved treatments for C3G, IC-MPGN, CFID 0 Note: aHUS = atypical Hemolytic Uremic Syndrome, C3G = Complement 3 Glomerulopathy, IC-MPGN = Immune-Complex Membranoproliferative Glomerulonephritis, CFID = Complement Factor I Deficiency References: Bresin et al. JASN. 2013; Fremeaux-Bacchi et al. ASN. 2013; Rui-Ru et al. Jour Rare Dis Res. 2018; Servais et al. Kidney Int. 2012; Iatropoulous et al. Mol Immunol. 2016; Hou et al. Kidney Int. 2014; Alba-Domiguez et al. J rare Dis. 2012. El Sissy et al. Front. Immunol. 2019; Shields et al. Front Immunol. 2019; Naesens et al. Jour Allergy & Clin Immunol. 2020. Yan et al. Clin Epi 2020; Smith et al. 22 Nature Reviews. 2019; Noris et al. Clin J Am Soc Nephrol. 2010; CBIO KOL interviews
C3b & C4b Degraders Expanding into classical complement disorders 23C3b & C4b Degraders Expanding into classical complement disorders 23
Dialing catalytic power & specificity into CFI Using ProTUNE™ engineering platform to tune C3b & C4b degraders Catalytic Activity Precision CFI Therapeutics Tunable potency to C3b/C4b control dysregulated Specificity complement Tunable specificity Desired toward C3b & C4b to Functionality restore the right balance C4b C3b to complement ProTUNE™ PLATFORM Tuned C3b-C4b Degrader 24Dialing catalytic power & specificity into CFI Using ProTUNE™ engineering platform to tune C3b & C4b degraders Catalytic Activity Precision CFI Therapeutics Tunable potency to C3b/C4b control dysregulated Specificity complement Tunable specificity Desired toward C3b & C4b to Functionality restore the right balance C4b C3b to complement ProTUNE™ PLATFORM Tuned C3b-C4b Degrader 24
C3b-C4b degraders significantly reduce inflammation in vivo Significantly decrease in inflammatory markers involved in IgA nephropathy Inflammatory markers in IgA nephropathy Rat model of complement-mediated inflammation ✱✱✱✱ 5000 100 ✱✱✱ 4000 80 3000 60 Baseline 2000 40 1000 20 Baseline 0 0 1, 2 Reduction of IFNγ & TNF⍺ involved in kidney damage & proteinuria in IgA nephropathy patients 1. Yano, N. et al. Phenotypic Characterization of Cytokine Expression in Patients With IgA Nephropathy. J Clin Immunol 17, 396–402 (1997). 2. Lim, C. S. et al. Th1/Th2 predominance and proinflammatory cytokines determine the clinicopathological severity of IgA nephropathy. Nephrol Dial Transpl 16, 269–275 (2001). Values are mean +/- SEM, ***p<0.001 using One Way or Two-way ANOVA. 25 Vehicle CB4775 Vehicle CB4775 IFNγ (pg/mL) TNFα (pg/mL)C3b-C4b degraders significantly reduce inflammation in vivo Significantly decrease in inflammatory markers involved in IgA nephropathy Inflammatory markers in IgA nephropathy Rat model of complement-mediated inflammation ✱✱✱✱ 5000 100 ✱✱✱ 4000 80 3000 60 Baseline 2000 40 1000 20 Baseline 0 0 1, 2 Reduction of IFNγ & TNF⍺ involved in kidney damage & proteinuria in IgA nephropathy patients 1. Yano, N. et al. Phenotypic Characterization of Cytokine Expression in Patients With IgA Nephropathy. J Clin Immunol 17, 396–402 (1997). 2. Lim, C. S. et al. Th1/Th2 predominance and proinflammatory cytokines determine the clinicopathological severity of IgA nephropathy. Nephrol Dial Transpl 16, 269–275 (2001). Values are mean +/- SEM, ***p<0.001 using One Way or Two-way ANOVA. 25 Vehicle CB4775 Vehicle CB4775 IFNγ (pg/mL) TNFα (pg/mL)
C3b-C4b degraders for IgA nephropathy patients Dual targeting of alternate & lectin pathways Classical Lectin Alternate Differentiation pathway pathway pathway + Dual targeting mode of action: lectin & C3(H O) alternate pathways MBL C1q 2 C1r Rationale for IgA nephropathy MASPs CFD CFB C1s Clinically validated + Both lectin & alternate pathways are Clinically validated target for IgAN target for IgAN involved in IgA nephropathy & correlate C4 C2 1, 2, 3 with severe clinical manifestation Clinically validated targets C3b Bb C4b 2b C3 + Inhibition of only MASP2 or Factor B may be insufficient to reduce proteinuria in IgA nephropathy patients C4b C3b ProTUNE™ PLATFORM 1. Medjeral-Thomas et al. Kidney International Reports (2018); 2. Bi et al. BMC Nephrology (2019); 3. Roos et al. J Am Soc Nephrol (2006) 26C3b-C4b degraders for IgA nephropathy patients Dual targeting of alternate & lectin pathways Classical Lectin Alternate Differentiation pathway pathway pathway + Dual targeting mode of action: lectin & C3(H O) alternate pathways MBL C1q 2 C1r Rationale for IgA nephropathy MASPs CFD CFB C1s Clinically validated + Both lectin & alternate pathways are Clinically validated target for IgAN target for IgAN involved in IgA nephropathy & correlate C4 C2 1, 2, 3 with severe clinical manifestation Clinically validated targets C3b Bb C4b 2b C3 + Inhibition of only MASP2 or Factor B may be insufficient to reduce proteinuria in IgA nephropathy patients C4b C3b ProTUNE™ PLATFORM 1. Medjeral-Thomas et al. Kidney International Reports (2018); 2. Bi et al. BMC Nephrology (2019); 3. Roos et al. J Am Soc Nephrol (2006) 26
C3b-C4b degraders for IgA nephropathy patients Disease in which both lectin & alternative pathways drive pathogenesis High unmet need – current treatments only addressing symptoms + Most common form of glomerulopathies worldwide Healthy IgAN + Accumulation & deposition of IgA immune complexes leading to deterioration of renal function + 10% patients with rapidly progressive glomerulonephritis + 40% of IgAN patients develop end stage renal disease over 20 years & need dialysis/renal transplant in order to survive + Significant burden on healthcare resources with an estimated cost of $49.2 billion in 2020 in the US 27C3b-C4b degraders for IgA nephropathy patients Disease in which both lectin & alternative pathways drive pathogenesis High unmet need – current treatments only addressing symptoms + Most common form of glomerulopathies worldwide Healthy IgAN + Accumulation & deposition of IgA immune complexes leading to deterioration of renal function + 10% patients with rapidly progressive glomerulonephritis + 40% of IgAN patients develop end stage renal disease over 20 years & need dialysis/renal transplant in order to survive + Significant burden on healthcare resources with an estimated cost of $49.2 billion in 2020 in the US 27
C3a & C5a Degraders For inflammatory disorders Structural model based on PDB 2XRC 28
Dialing catalytic power & specificity to restore immunoregulation Using the ImmunoTUNE™ engineering platform to tune C3a & C5a degraders Mast Cell & Neutrophil Disorders Precision CFx Therapeutics Tunable potency for ANCA-AAV AK/VK different level of immunomodulation BP IPF Tunable specificity C3a C5a Asthma RA toward C3a & C5a to restore the right balance Anaphylaxis Cancer ImmunoTUNE™ to complement PLATFORM CD IBS 1 molecule can degrade 1000s of target molecules Mastocytosis ANCA-AAV, anti-neutrophil cytoplasmic-antibody-associated vasculitis; IBS, inflammatory Bowel Syndrome; CD, Crohn’s disease; RA, rheumatoid arthritis; BP, bullous pemphigoid; IPF, idiopathic pulmonary fibrosis; AK, Atopic keratoconjunctivitis; VK, vernal keratoconjunctivitis 29Dialing catalytic power & specificity to restore immunoregulation Using the ImmunoTUNE™ engineering platform to tune C3a & C5a degraders Mast Cell & Neutrophil Disorders Precision CFx Therapeutics Tunable potency for ANCA-AAV AK/VK different level of immunomodulation BP IPF Tunable specificity C3a C5a Asthma RA toward C3a & C5a to restore the right balance Anaphylaxis Cancer ImmunoTUNE™ to complement PLATFORM CD IBS 1 molecule can degrade 1000s of target molecules Mastocytosis ANCA-AAV, anti-neutrophil cytoplasmic-antibody-associated vasculitis; IBS, inflammatory Bowel Syndrome; CD, Crohn’s disease; RA, rheumatoid arthritis; BP, bullous pemphigoid; IPF, idiopathic pulmonary fibrosis; AK, Atopic keratoconjunctivitis; VK, vernal keratoconjunctivitis 29
C3a-C5a degraders: Efficacy in an acute LPS-induced ARDS model CFx improves respiratory function & reduces cell infiltrates Respiratory functions & cell infiltration at 24 h Mouse LPS model of lung inflammation ✱ ✱ 9 1000 3×10 800 9 2×10 600 CFx 7-fold lower dose vs. 400 9 1×10 anti-C5 200 0 0 CFx outperforms anti-C5 antibody in reducing inflammatory cell infiltration CFx compares well on respiratory functions with anti-C5 antibody 30 Vehicle CPN-HSA CFx Anti-C5 Ab Vehicle CPN-HSA CFx Anti-C5 Ab PenH (% change from baseline) Leukocyte CountC3a-C5a degraders: Efficacy in an acute LPS-induced ARDS model CFx improves respiratory function & reduces cell infiltrates Respiratory functions & cell infiltration at 24 h Mouse LPS model of lung inflammation ✱ ✱ 9 1000 3×10 800 9 2×10 600 CFx 7-fold lower dose vs. 400 9 1×10 anti-C5 200 0 0 CFx outperforms anti-C5 antibody in reducing inflammatory cell infiltration CFx compares well on respiratory functions with anti-C5 antibody 30 Vehicle CPN-HSA CFx Anti-C5 Ab Vehicle CPN-HSA CFx Anti-C5 Ab PenH (% change from baseline) Leukocyte Count
C3a-C5a degraders: Potential for ANCA-AAV patients Dual targeting of both C3a & C5a with one protease medicine Classical pathway Lectin pathway Alternate pathway Differentiation + Degrade activation products of C3 (C3a) & C5 (C5a) that are inflammatory mediators C3 convertase + May provide beneficial function via C5L2 pathway C3 Rationale for ANCA-AAV C3a C3b + Both C3a & C5a are higher in active AAV 1, 2 patients C3aR C3 convertase Clinically validated targets C5aR + Inhibition of C5a or C5aR may be C5 C3a C5a insufficient to increase remission rates in ImmunoTUNE™ C5a C5b PLATFORM ANCA-AAV patients Clinically validated targets for ANCA 1. S. Moiseev et al. British Society for Immunology, Clinical and Experimental Immunology (2020); 2. Gou et al. Kidney International (2012). 31C3a-C5a degraders: Potential for ANCA-AAV patients Dual targeting of both C3a & C5a with one protease medicine Classical pathway Lectin pathway Alternate pathway Differentiation + Degrade activation products of C3 (C3a) & C5 (C5a) that are inflammatory mediators C3 convertase + May provide beneficial function via C5L2 pathway C3 Rationale for ANCA-AAV C3a C3b + Both C3a & C5a are higher in active AAV 1, 2 patients C3aR C3 convertase Clinically validated targets C5aR + Inhibition of C5a or C5aR may be C5 C3a C5a insufficient to increase remission rates in ImmunoTUNE™ C5a C5b PLATFORM ANCA-AAV patients Clinically validated targets for ANCA 1. S. Moiseev et al. British Society for Immunology, Clinical and Experimental Immunology (2020); 2. Gou et al. Kidney International (2012). 31
C3a-C5a degraders: Potential for ANCA-AAV patients Autoimmune disease where anaphylatoxins play a role in the pathogenesis High unmet need – current treatments only addressing symptoms + Autoimmune disorder characterized by inflammation & destruction of small blood vessels + Clinical signs vary & affect several organs with frequent involvement of upper respiratory track & kidneys + Severe pain due to neuropathy, pulmonary hemorrhages, failure of kidneys st + 10-15% of patients die in the 1 year of treatment with conventional therapies (immunosuppressant & glucocorticoid) + The only treatments available are to manage the symptoms 1. S. Moiseev et al. British Society for Immunology, Clinical and Experimental Immunology (2020); 2. Gou et al. Kidney International (2012). 32C3a-C5a degraders: Potential for ANCA-AAV patients Autoimmune disease where anaphylatoxins play a role in the pathogenesis High unmet need – current treatments only addressing symptoms + Autoimmune disorder characterized by inflammation & destruction of small blood vessels + Clinical signs vary & affect several organs with frequent involvement of upper respiratory track & kidneys + Severe pain due to neuropathy, pulmonary hemorrhages, failure of kidneys st + 10-15% of patients die in the 1 year of treatment with conventional therapies (immunosuppressant & glucocorticoid) + The only treatments available are to manage the symptoms 1. S. Moiseev et al. British Society for Immunology, Clinical and Experimental Immunology (2020); 2. Gou et al. Kidney International (2012). 32
Degraders Protease platforms for complement homeostasis & immunomodulation 33Degraders Protease platforms for complement homeostasis & immunomodulation 33
Our protease platforms are tailored to specific indications Tuning functionality to restore complement homeostasis & immunoregulation ProTUNE™ ImmunoTUNE™ Nephrology Hematology C3b-C4b C3a-C5a oncology Neurology C4b C3a C3b C5a ProTUNE™ ImmunoTUNE™ PLATFORM PLATFORM Immunology Autoimmune 34
CB 4332 spearheads a deep pipeline in complement Next development candidate in 2022 Indication 2021 2022 CFI Deficiency Screening & Natural History Study CB 4332 Natural History Preclinical IND Phase I CFI Deficiency CB 4332 Biomarker Data Partial Deficiency Phase I/II CB 4332 IC-MPGN/aHUS/C3G Non-Deficiency Indication Selection Phase I/II CB 4332 Expansion Indications Discovery IgA Nephropathy C3b-C4b Development Candidates for Each Program Discovery ANCA-AAV C3a-C5a 35 Platform CFI-HSA Technology Replacement
Milestones Clinton Musil | CFO Closing Remarks, Q&AMilestones Clinton Musil | CFO Closing Remarks, Q&A
Milestones: Catalyst Biosciences complement programs Enrollment to Observational trial for CB 4332 start mid-2021 2021 Progress CB 2782-PEG in collaboration with Biogen Mid-2022 CB 4332 in the clinic globally 2022 Development candidates in lead discovery programs 2022 Open-label PK & biomarker data for CB 4332 37Milestones: Catalyst Biosciences complement programs Enrollment to Observational trial for CB 4332 start mid-2021 2021 Progress CB 2782-PEG in collaboration with Biogen Mid-2022 CB 4332 in the clinic globally 2022 Development candidates in lead discovery programs 2022 Open-label PK & biomarker data for CB 4332 37
The Protease Medicines Company Harnessing the catalytic power of proteases Novel differentiated medicines Robust complement portfolio Clinical-stage assets Unique expertise in protease engineering 38The Protease Medicines Company Harnessing the catalytic power of proteases Novel differentiated medicines Robust complement portfolio Clinical-stage assets Unique expertise in protease engineering 38
