Catalyst Biosciences 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

CATALYST BIOSCIENCES Catalyst

Biosciences Corporate Overview 26 January 2021 Exhibit 99.1

Catalyst Biosciences 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, potential markets for and advantages of MarzAA and DalcA; plans to enroll a pivotal Phase 3 registration study of MarzAA; the initiation of a

Phase 1/2 trial in patients with FVII Deficiency, Glanzmann Thrombasthenia, and patients treated with Hemlibra; MarzAA as possibly the first prophylactic for FVII Deficiency and Glanzmann Thrombasthenia; the potential for MarzAA and DalcA to

effectively and therapeutically treat hemophilia subcutaneously; projected complement market opportunity, solution to fundamental shortcomings in current treatment options, plans to enroll the CB 4332 observational trial in

the Company's complement program in mid-2021, and ongoing updates related to CB 4322 and the C4b degrader. 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, that human trials will not replicate the results from earlier trials, 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 February 20, 2020, Quarterly Report on Form 10-Q

filed with the SEC on November 5, 2020, 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.

Late-stage asset in Phase 3 Robust

complement portfolio Clinical-stage hemophilia assets Novel differentiated protease medicines Harnessing the catalytic power of proteases The Protease Medicines Company Catalyst Biosciences

Catalyst Biosciences

Catalyst's protease platform generates differentiated therapeutics Unique expertise in protease biology enables design of optimized protease therapeutics Functionally enhance natural proteases in the complement & coagulation cascades

Engineer novel protein degraders in the complement cascade Modulate or target biological activation or inactivation Protease scaffold Therapeutic protease Structure guided design Pharmacokinetic improvement Molecular evolution Our proteases

Discovery platform Engineered regulation

Catalyst Biosciences Proteases

are ideal for high abundancy targets & cascades A better way to regulate biological processes compared with antibodies & small molecules Efficient regulation at low concentrations of therapeutic protease Requires high concentrations in

excess of the target Requires high concentrations & frequent dosing Antibodies Small molecules / peptides Proteases

R PC P1/2 P2 P3 Catalyst

Biosciences Pipeline Hemostasis SQ Marzeptacog alfa (FVIIa) "MarzAA" Hemophilia A or B with inhibitors - ToB FVIID/Glanzmann/Hemlibra - ToB Complement IVT CB 2782-PEG C3 degrader for Dry AMD SQ CB 4332 Enhanced CFI C4b Degrader

Additional programs Hemostasis SQ Dalcinonacog alfa (FIX) "DalcA" Hemophilia B CB 2679d-GT Hemophilia B FIX Gene Therapy

Catalyst Biosciences Clinical

& partnering success of the CBIO protease platform Before treatment On treatment Marzeptacog alfa Dalcinonacog alfa CB 2782-PEG Engineered rFVIIa protease 90% reduction in annualized bleed rate Achieved sustained & high target levels of FIX

Best-in-class profile for dry AMD Extended pharmacodynamics Engineered rFIX protease Novel C3 degrader 50% 5% 1% Mild Hemophilia Normal clotting levels Severe Hemophilia Moderate Hemophilia

Catalyst Biosciences Addresses a

clear unmet need in hemophilia & other bleeding disorders Marzeptacog alfa (activated) - MarzAA: SQ rFVIIa 9-fold higher activity vs NovoSeven RT Potency allows for SQ dosing that prolongs half-life Simple, small volume SQ administration

Preclinical efficacy of SQ on-demand treatment HA mouse after tail cut; HA dog; HA rat P2/3 prophylaxis efficacy & safety in HA or HB with inhibitors 46 patients treated including: single dose IV, up to 3 SQ doses/day, & daily SQ up to 97

days - no ADA FDA Fast Track designation for treatment of episodic bleeding in Hem A or B with inhibitors Granted on 2 December 2020 P129A M298Q T128N Increased procoagulant activity Q286R

Catalyst Biosciences SQ MarzAA

is a large commercial opportunity SQ MarzAA has a superior profile Global NovoSeven sales breakdown by indication (2019) Faster & easier to administer vs N7 dosed every 2 hours IV until hemostasis MarzAA SQ half-life ~8x longer than N7 Potential

to reduce rebleeding Can be combined with Hemlibra in vitro without increased thrombogenicity Ideal for pediatrics and patients with venous access issues Prophylaxis efficacy demonstrated in P2 Hem A Inh (47%) Other (22%) Glanzmann (7%) Source:

Adivo Associates market research; Catalyst Biosciences market research. Data on file Hem B Inh (11%) FVII Def (5%) AHA (8%)

Catalyst Biosciences MarzAA

could be the first prophylactic for Glanzmann & FVIID Global NovoSeven on demand sales Glanzmann Thrombasthenia, FVIID Unmet need in prophylaxis Growing number of Glanzmann Thrombasthenia and FVIID patients treated with NovoSeven Source:

Catalyst Biosciences, Adivo Associates Market Research, Data on file. *Note: Treated patients may be counted multiple times as patients may have multiple bleeding events per year needing factor treatment 9% total increase in patients over 3 years

Catalyst Biosciences Unmet

need in treatment of a bleed Source: 1NovoSeven PI Rev 7/2020; 2Adivo Associates market research; 3Catalyst Biosciences market research; Data on file; Neuman et al. ISTH 2020 Patients reported needing an average of 6 hours and 3 infusions of

NovoSeven to resolve bleeds Some bleeds take longer than 72 hours to resolve1,2,3 NovoSeven Current bypass agents require multiple infusions over the course of hours MAA-102: PK MarzAA levels support SQ ToB Target levels are rapidly achieved Target

levels can be maintained for 18 hours with a single SQ dose of 60 g/kg MarzAA Clinical PK MarzAA levels support SQ ToB

Catalyst Biosciences

Hemophilia A or B with inhibitors, ABR 8 Crimson 1 Phase 3 study: Treatment of episodic bleeding MarzAA SQ 60 g/kg 1-3 doses 130 bleeds per sequence 5 bleeds per patient N = 30 SOC IV 1-3 doses 5 bleeds per patient 114

bleeds per sequence MarzAA SQ 60 g/kg 1-3 doses 5 bleeds per patient 114 bleeds per sequence 130 bleeds per sequence 5 bleeds per patient SOC IV 1-3 doses N = 30 Primary endpoint Non-inferior hemostatic efficacy: standard 4-point

scale at 24 h Secondary endpoints Time to bleed resolution; number of doses; rescue meds Safety Adverse events, anti-drug antibodies (ADA); thrombosis Statistics + SOC estimate 85% Excellent/good treatment of bleeds + Non-inferiority margin of 12% +

2.5% significance, one-sided + 90% power

Catalyst Biosciences FVII

deficiency, Glanzmann Thrombasthenia and HA on Hemlibra: N = 8 each MAA-202 Phase 1/2 study design Phase 1 Primary endpoint: Pharmacokinetics Secondary endpoint: Pharmacodynamics Phase 2 ToB Primary endpoint: Hemostatic efficacy at 24 hours

Secondary endpoints: Effective hemostasis at successive timepoints; doses needed; rescue meds Safety: Adverse events and ADA Single dose Single dose escalation GT 30 bleeds FVIID 30 bleeds Phase 2 ToB Phase 1 PK MarzAA IV each cohort

MarzAA SQ HA 15 bleeds MarzAA SQ 1-3 doses Multiple dose Q3H

Catalyst Biosciences

CBIO's complement pipeline CB 2782 Novel engineered C3 degrader established CBIO in complement CB 4332 Leads CBIO's expansion into systemic complement in CFI dysregulation Next generation of specific and potent C4b degraders targets

classical complement disorders with large market potential Future complement degraders broaden CBIO's footprint 2 3 4 1 CB 4332 C4b Degraders NextGen Degraders CB 2782

Catalyst Biosciences

Complement is a perfect fit to develop protease therapeutics The complement pathway is driven by a protease cascade Reference: Figure adapted from Mastellos et al., Clinical promise of next-generation complement therapeutics. Nature Reviews. 2019 of

the complement cascade is regulated by proteases 80 % Exacerbation Immune modulation Immune modulation C1qR C3aR C1s C1r AAb NAb Neoepitopes/ autoepitopes Damaged/altered/foreign cells and debris C1-INH C2 C4 C4a C4b2b C3 Extrinsic protease C3a

C3a-dR CPN C3b C4b2b3b C3bBb3b C5 convertase C5 C5b C5a Chemotaxis, inflammatory signaling and cell activation C5aR2 C5aR1 C5a-dR CPN MAC C6 C7 C8 C9n Extrinsic proteases CD59 MBL Fcn CL MASP1 MASP2 C1q Tick-over C3*Bb C3bBb pFD FP FP FD FB FH FP

MASP3 C3* C3 C3b FP ? ? FB FD C3bBb C3 convertase FP FD FB FH CD55 CR1 C3b iC3b CD46 FH FI CR1 C3dg FI CR1 CR2 CR4 CR3 CR1 CR46 Exacerbation DAMP Amplification Immune modulation Adhesion Phagocytosis Trafficking Signaling Adaptive signaling Lysis,

cell damage Terminal pathway Breakdown pathway CP LP AP Circulation turnover FI FI C4BP FI FH FI FI FH

Catalyst Biosciences

Complement plays a critical role in many diseases Nephrology Hematology/Oncology Endocrine/Metabolism Infectious Disease Cardiovascular Dermatology Neurology Musculoskeletal Immunology Ophthalmology Pulmonology Gastroenterology References:

Globaldata consensus net sales forecast 2020 Late-stage complement therapies projected to achieve net sales over $12B by 2026

Catalyst Biosciences CBIO is

taking a targeted approach to complement regulation Classical pathway Lectin pathway Alternative pathway Membrane attack complex (MAC) Immune response inflammation C3a C5a C5b C3 C5 C3b CB 2782-PEG C4b MASP C4 C2 C1r C1s C3b C3 (H2O) FD FB CB 4332:

Enhanced CFI C4b Degrader C3b FD FB Engineered proteases address the root cause of the pathology Current C5 blockade therapies do not address disease root cause leading to inadequate disease control The catalytic power of proteases provides

advantages over small molecules and antibodies

Catalyst Biosciences Protease

advantage demonstrated in vivo CB 2782-PEG - designed as a best-in-class C3 degrader in dry AMD CB 2782-PEG degrades C3 levels in the eye for at least 28 days in a non-human primate model Catalytic advantage of proteases One therapeutic

molecule neutralizes 1000s Fast & potent response Extended pharmacodynamic effect Can activate or degrade therapeutic targets Engineered novel protein degraders "sweep away" difficult to drug targets

Catalyst Biosciences CB

2782-PEG long acting anti-C3 protease Geographic atrophy in dry AMD can result in blindness Advanced stage of dry age-related macular degeneration (dAMD) dAMD affects ~1M people in the US & >5M WW, no currently approved therapy Global market

~ >$5B C3 is a clinically validated target (randomized P2) for the treatment of dAMD Best-in-class C3 degrader for dry AMD Generated from Catalyst's proprietary protease engineering platform Potent, selective & long acting, degrades C3

into inactive fragments Preclinical NHP PK & PD data* predict best-in-class human intravitreal dosing 3 or 4 times a year *Furfine et al. ARVO 2019 Biogen collaboration $15M upfront, up to $340M in milestones and tiered royalties up to low

double digits Catalyst: fully funded pre-clinical and manufacturing activities Biogen: IND-enabling activities, WW clinical development & commercialization

Classical pathway Alternative

pathway Catalyst Biosciences Normal CFI: Key central regulator of complement activation C4 C2 C1r C1s C3b C3 (H2O) FD FB CFI's role is down-regulation of C4b & C3b Inhibition of C4b and C3b prevents overactivation of the complement

responses that can cause disease C4b CFI

Classical pathway Alternative

pathway Membrane attack complex (MAC) Immune response inflammation Catalyst Biosciences CFI dysregulation: Lack of proteolytic CFI activity causes disease C3a C5a C5b C3 C5 C3b C4b C4 C2 C1r C1s C3b C3 (H2O) FD FB CFI Defective CFI In

patients with CFI mutations, C4b and C3b cannot be sufficiently regulated Dysregulation leads to overactivation of the complement pathway and damaging immune responses

Classical pathway Alternative

pathway Catalyst Biosciences CB 4332 - CBIO's enhanced CFI Specifically addresses the problem by restoring CFI regulation C4 C2 C1r C1s C3b C3 (H2O) FD FB CB 4332: Enhanced CFI C4b

Catalyst Biosciences CB 4332:

Enhanced Complement Factor I CBIO's next SQ development candidate to restore CFI regulation References: 1Bienaime et al. Kidney Int. 2010; 2Ferreira et al. Nefrologia. 2016; Note: CFH = Complement factor H; Structural model

based on PDB 2XRC. . Restores normal complement system in patients with dysregulated CFI No specific therapies exist to correct CFI dysregulation Targets population with no treatment or who respond poorly to current

treatments1,2 Genetically defined patient population Rationale & unmet need Half-life extension technology Engineered for an extended half-life Once weekly SQ therapy - no PEG Full activity comparable to native CFI Classical and

alternative pathway regulation Efficient high yield production process

Catalyst Biosciences CB 4332

& plasma CFI perform similarly in human serum Inhibition of hemolysis (%) Concentration of test article (nM) Concentration of test article (nM) Inhibition of hemolysis (%) Classical pathway Alternative pathway

Catalyst Biosciences Diseases

with CFI mutations have tremendous potential aHUS C3G IC-MPGN Geographic atrophy CFI Deficiency $500M $10B+ Current development targets Potential targets Chronic inflammation Recurrent infections Autoimmune disorders

Catalyst Biosciences 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. Nature Reviews. 2019; Noris et al. Clin J Am Soc Nephrol. 2010; CBIO KOL interviews aHUS C3G IC-MPGN US / EU5 market opportunity Market

opportunity in CFI deficient aHUS, C3G, IC-MPGN $500M Additional opportunity in CFI Deficiency outside nephrology Significant opportunity for patients with CFI mutations 0 Specific systemic therapies in development for patients with dysregulated CFI