Exhibit 99.1 MOLECULAR TEMPLATES Corporate Presentation I January 2021 (NASDAQ: MTEM) Exhibit 99.1 MOLECULAR TEMPLATES Corporate Presentation I January 2021 (NASDAQ: MTEM)

Forward-Looking Statements Except for statements of historical fact, the statements in this presentation are forward-looking statements, including, but not limited to, statements regarding the future development of our proprietary Engineered Toxin Body (ETB) technology; statements relating to the potential lifting of the partial clinical hold on our MT-3724 clinical trials; statements relating to the development of the MT-3724, MT-5111, TAK-169, and MT-6402, and our preclinical pipeline; our utilization of a next-generation ETB scaffold that has been designed to reduce or eliminate the propensity for innate immunity, including CLS, and to reduce the propensity for aggregation; our plans to enter the clinic with multiple candidates; our expected receipt of clinical data; and our future cash needs. These statements constitute forward-looking statements within the meaning of Section 27A of the Securities Act and Section 21E of the Securities Exchange Act and are usually identified by the use of words such as anticipates, believes, estimates, expects, intends, may, plans, projects, seeks, should, will, and variations of such words or similar expressions. These forward- looking statements reflect our current views about our plans, intentions, expectations, strategies and prospects, which are based on the information currently available to us and on assumptions we have made. Although we believe that our plans, intentions, expectations, strategies and prospects as reflected in or suggested by those forward-looking statements are reasonable, we can give no assurance that the plans, intentions, expectations or strategies will be attained or achieved. Furthermore, actual results may differ materially from those described in the forward-looking statements and will be affected by a variety of risks and factors that are beyond our control. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Important factors that may cause actual results to differ materially from the results discussed in the forward-looking statements include risks and uncertainties, including (1) our failure to secure and maintain relationships with collaborators; (2) risks relating to clinical trials and other uncertainties of product candidate development; (3) our ability to successfully resolve the partial clinical hold with regard to MT-3724; (4) risks relating to the commercialization, if any, of our proposed product candidates (such as marketing, regulatory, product liability, supply, competition, and other risks); (5) dependence on the efforts of third parties including our strategic partners; (6) dependence on intellectual property; and (7) risks from global pandemics including COVID-19. Further information regarding these and other risks is included under the heading Risk Factors in our filings with the Securities and Exchange Commission available from the SEC's website (www.sec.gov). Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. These forward looking statements reflect management’s current views and we do not undertake to update any of these forward-looking statements to reflect a change in events or circumstances that occur after the date of this presentation except as required by law. MOLECULAR TEMPLATES 2021 Corporate Presentation I 2Forward-Looking Statements Except for statements of historical fact, the statements in this presentation are forward-looking statements, including, but not limited to, statements regarding the future development of our proprietary Engineered Toxin Body (ETB) technology; statements relating to the potential lifting of the partial clinical hold on our MT-3724 clinical trials; statements relating to the development of the MT-3724, MT-5111, TAK-169, and MT-6402, and our preclinical pipeline; our utilization of a next-generation ETB scaffold that has been designed to reduce or eliminate the propensity for innate immunity, including CLS, and to reduce the propensity for aggregation; our plans to enter the clinic with multiple candidates; our expected receipt of clinical data; and our future cash needs. These statements constitute forward-looking statements within the meaning of Section 27A of the Securities Act and Section 21E of the Securities Exchange Act and are usually identified by the use of words such as anticipates, believes, estimates, expects, intends, may, plans, projects, seeks, should, will, and variations of such words or similar expressions. These forward- looking statements reflect our current views about our plans, intentions, expectations, strategies and prospects, which are based on the information currently available to us and on assumptions we have made. Although we believe that our plans, intentions, expectations, strategies and prospects as reflected in or suggested by those forward-looking statements are reasonable, we can give no assurance that the plans, intentions, expectations or strategies will be attained or achieved. Furthermore, actual results may differ materially from those described in the forward-looking statements and will be affected by a variety of risks and factors that are beyond our control. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Important factors that may cause actual results to differ materially from the results discussed in the forward-looking statements include risks and uncertainties, including (1) our failure to secure and maintain relationships with collaborators; (2) risks relating to clinical trials and other uncertainties of product candidate development; (3) our ability to successfully resolve the partial clinical hold with regard to MT-3724; (4) risks relating to the commercialization, if any, of our proposed product candidates (such as marketing, regulatory, product liability, supply, competition, and other risks); (5) dependence on the efforts of third parties including our strategic partners; (6) dependence on intellectual property; and (7) risks from global pandemics including COVID-19. Further information regarding these and other risks is included under the heading Risk Factors in our filings with the Securities and Exchange Commission available from the SEC's website (www.sec.gov). Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. These forward looking statements reflect management’s current views and we do not undertake to update any of these forward-looking statements to reflect a change in events or circumstances that occur after the date of this presentation except as required by law. MOLECULAR TEMPLATES 2021 Corporate Presentation I 2

MTEM: Developing Novel Therapeutics With a Unique Platform Unique MOA Global Partners Engineered Toxin Bodies (ETBs) have the specificity of an Takeda: CD38 co-development, multi-target collaboration, equity antibody, can induce their own internalization, and act through a investment. Vertex: Multi-target collaboration around potent and unique mechanism of action: ribosomal destruction myeloablation, equity investment Advancing Pipeline Future Opportunities st POC with 1 -Gen ETB demonstrating forced internalization, ETB platform provides continued pipeline opportunities via nd partnerships and internal development. Next-Gen ETBs in preclinical efficacy, and safety. Two 2 -Gen ETBs in clinic with improved rd development against targets including CTLA-4, SLAMF-7, CD45 efficacy and safety. FPI with 3 -Gen ETB targeting PD-L1 in 1H21. Known Targets for Early Signs of Safety & Efficacy Strong Cash Position ETBs against validated targets can provide evidence of Current cash funds operations into 2H22 without additional safety and response as early as Phase 1 business development MOLECULAR TEMPLATES 2021 Corporate Presentation I 3MTEM: Developing Novel Therapeutics With a Unique Platform Unique MOA Global Partners Engineered Toxin Bodies (ETBs) have the specificity of an Takeda: CD38 co-development, multi-target collaboration, equity antibody, can induce their own internalization, and act through a investment. Vertex: Multi-target collaboration around potent and unique mechanism of action: ribosomal destruction myeloablation, equity investment Advancing Pipeline Future Opportunities st POC with 1 -Gen ETB demonstrating forced internalization, ETB platform provides continued pipeline opportunities via nd partnerships and internal development. Next-Gen ETBs in preclinical efficacy, and safety. Two 2 -Gen ETBs in clinic with improved rd development against targets including CTLA-4, SLAMF-7, CD45 efficacy and safety. FPI with 3 -Gen ETB targeting PD-L1 in 1H21. Known Targets for Early Signs of Safety & Efficacy Strong Cash Position ETBs against validated targets can provide evidence of Current cash funds operations into 2H22 without additional safety and response as early as Phase 1 business development MOLECULAR TEMPLATES 2021 Corporate Presentation I 3

ETBs: Novel Mechanisms of Action in Oncology ETBs use an antibody domain for targeting genetically fused to a Engineered Toxin Bodies de-immunized SLTA − ETBs can be made to bind any extracellular target st rd nd 1 Gen 3 Gen 2 Gen − ETBs retain the SLTA-mediated: Engineered Engineered SLTA SLTA • Internalization (even against non-internalizing targets) SLTA SLTA SLTB (CD77 scFv scFv • Routing to the cytosol scFv ligand) AST • Enzymatic and irreversible destruction of ribosome Iterative improvements made to ETB scaffold st − Clinical validation of forced internalization, safety, and efficacy with 1 -Gen ETB (MT-3724) nd − 2 -Gen ETBs have been engineered to have: • Increased potency • Decreased adaptive immunity • Decreased innate immunity via reduced TLR4 affinity • Reduced propensity for aggregation rd nd − 3 -Gen ETBs have all the properties of the 2 -Gen and can specifically alter the immunophenotype of tumor cells via antigen seeding technology (AST) MOLECULAR TEMPLATES 2021 Corporate Presentation I 4ETBs: Novel Mechanisms of Action in Oncology ETBs use an antibody domain for targeting genetically fused to a Engineered Toxin Bodies de-immunized SLTA − ETBs can be made to bind any extracellular target st rd nd 1 Gen 3 Gen 2 Gen − ETBs retain the SLTA-mediated: Engineered Engineered SLTA SLTA • Internalization (even against non-internalizing targets) SLTA SLTA SLTB (CD77 scFv scFv • Routing to the cytosol scFv ligand) AST • Enzymatic and irreversible destruction of ribosome Iterative improvements made to ETB scaffold st − Clinical validation of forced internalization, safety, and efficacy with 1 -Gen ETB (MT-3724) nd − 2 -Gen ETBs have been engineered to have: • Increased potency • Decreased adaptive immunity • Decreased innate immunity via reduced TLR4 affinity • Reduced propensity for aggregation rd nd − 3 -Gen ETBs have all the properties of the 2 -Gen and can specifically alter the immunophenotype of tumor cells via antigen seeding technology (AST) MOLECULAR TEMPLATES 2021 Corporate Presentation I 4

MT-3724 st 1 -Gen ETB Targeting CD20 for LymphomasMT-3724 st 1 -Gen ETB Targeting CD20 for Lymphomas

st MT-3724: 1 -Gen CD20-Targeted ETB C D 2 0 TA R G E T E D Single-chain variable fragment (scFv) MT-3724 with specificity to CD20 O T H E R P R O P E R T I E S Fusion protein; no linker chemistry. Short serum half-life; irreversible intra-cellular effects. CD20 binding scFv F O R C E D TA R G E T I N T E R N A L I Z AT I O N First agent to demonstrate efficient internalization against CD20, a non-internalizing receptor N O V E L E N Z Y M AT I C WT SLTA Payload P AY L O A D Primary mechanism of cell-kill is enzymatic ribosome destruction st W I L D - T Y P E P AY L O A D 1 -Gen ETB • Not de-immunized Wild-type Shiga-like toxin A-subunit • Less potent than next-gen ETBs payload. Retains TLR4 interaction • Propensity for aggregation MOLECULAR TEMPLATES 2021 Corporate Presentation I 6st MT-3724: 1 -Gen CD20-Targeted ETB C D 2 0 TA R G E T E D Single-chain variable fragment (scFv) MT-3724 with specificity to CD20 O T H E R P R O P E R T I E S Fusion protein; no linker chemistry. Short serum half-life; irreversible intra-cellular effects. CD20 binding scFv F O R C E D TA R G E T I N T E R N A L I Z AT I O N First agent to demonstrate efficient internalization against CD20, a non-internalizing receptor N O V E L E N Z Y M AT I C WT SLTA Payload P AY L O A D Primary mechanism of cell-kill is enzymatic ribosome destruction st W I L D - T Y P E P AY L O A D 1 -Gen ETB • Not de-immunized Wild-type Shiga-like toxin A-subunit • Less potent than next-gen ETBs payload. Retains TLR4 interaction • Propensity for aggregation MOLECULAR TEMPLATES 2021 Corporate Presentation I 6

MT-3724: Activity Demonstrated in DLBCL Phase 1/1b study conducted in heavily pretreated B-cell lymphoma patients • Median age of 65 • Median of 4 prior NHL therapies; median of 2 prior anti-CD20 Mabs Patients evaluable for efficacy in phase I (n=25) DLBCL or Mixed DLBCL/FL (n=19) Deep and prolonged dose-dependent B-cell depletion observed Low serum RTX levels (n=13) Favorable tolerability profile 2 Complete Responses (CR) • Maximum tolerated dose (MTD) established at 50 µg/kg 1 Complete Metabolic Response (CMR) - Dose cohorts of 5, 10, 20, 50, 75, and 100 µg/kg evaluated 2 Partial Responses (PR) • Dose-limiting toxicities (DLTs) were non-life threatening grade 2/3 events including grade 2 capillary leak syndrome (CLS) which resolved upon 3 Stable Disease (SD) (49%, 47% tumor reduction) cessation of dosing; CLS did not recur upon re-challenge at lower doses 5 Progressive Disease (PD) ® High serum levels of Rituxan (RTX) inhibits MT-3724 activity 38% Objective Response Rate (ORR)a • 0/6 response rate 60% ORR at MTD: 2 CRs, 1 PR, 2 PD • Patients screened out for high RTX in ongoing studies Median number of prior therapies in responders was 3; responses seen in R-CHOP refractory pts. Includes 2 stable disease patients who had 49% and 47% tumor reductions MOLECULAR TEMPLATES 2021 Corporate Presentation I 7MT-3724: Activity Demonstrated in DLBCL Phase 1/1b study conducted in heavily pretreated B-cell lymphoma patients • Median age of 65 • Median of 4 prior NHL therapies; median of 2 prior anti-CD20 Mabs Patients evaluable for efficacy in phase I (n=25) DLBCL or Mixed DLBCL/FL (n=19) Deep and prolonged dose-dependent B-cell depletion observed Low serum RTX levels (n=13) Favorable tolerability profile 2 Complete Responses (CR) • Maximum tolerated dose (MTD) established at 50 µg/kg 1 Complete Metabolic Response (CMR) - Dose cohorts of 5, 10, 20, 50, 75, and 100 µg/kg evaluated 2 Partial Responses (PR) • Dose-limiting toxicities (DLTs) were non-life threatening grade 2/3 events including grade 2 capillary leak syndrome (CLS) which resolved upon 3 Stable Disease (SD) (49%, 47% tumor reduction) cessation of dosing; CLS did not recur upon re-challenge at lower doses 5 Progressive Disease (PD) ® High serum levels of Rituxan (RTX) inhibits MT-3724 activity 38% Objective Response Rate (ORR)a • 0/6 response rate 60% ORR at MTD: 2 CRs, 1 PR, 2 PD • Patients screened out for high RTX in ongoing studies Median number of prior therapies in responders was 3; responses seen in R-CHOP refractory pts. Includes 2 stable disease patients who had 49% and 47% tumor reductions MOLECULAR TEMPLATES 2021 Corporate Presentation I 7

MT-3724: Update on Partial Clinical Hold ● One subject death occurred on 20-Oct-2020 in the MT-3724 monotherapy study due to grade 5 capillary leak syndrome (CLS) − Subject was a seventh line DLBCL patient (ex-US site) who had rapidly progressed through three lines of therapy (including a first- generation CAR-T) in the six months prior to MT-3724 dosing − Subject experienced grade 2 CLS after two doses of MT-3724 which had resolved prior to resuming dosing ● First grade 5 CLS event across all MT-3724 studies − All prior occurrences of CLS across all MT-3724 studies were grade 2 or below ● Elevated C exposure observed in last 5 of 6 subjects dosed on MT-3724 monotherapy study max − Higher than expected pharmacokinetic (beyond pharmacokinetic projections) observed in these 5 subjects − All five subjects received drug from the same single lot of MT-3724 drug product − C exposures observed in these five subjects were higher than has been observed in any other subjects or studies with MT-3724 max nd − Elevated C exposures have not been observed with 2 generation ETB programs max ● Investigation ongoing and MT-3724 studies put on partial clinical hold by the FDA on Nov 4, 2020 − No new enrollment; patients on drug and benefiting will continue to receive MT-3724; lot in question held until investigation is complete ● Other MTEM studies continue and are not affected − TAK169, MT-5111 and planned MT-6402 MOLECULAR TEMPLATES 2021 Corporate Presentation I 8MT-3724: Update on Partial Clinical Hold ● One subject death occurred on 20-Oct-2020 in the MT-3724 monotherapy study due to grade 5 capillary leak syndrome (CLS) − Subject was a seventh line DLBCL patient (ex-US site) who had rapidly progressed through three lines of therapy (including a first- generation CAR-T) in the six months prior to MT-3724 dosing − Subject experienced grade 2 CLS after two doses of MT-3724 which had resolved prior to resuming dosing ● First grade 5 CLS event across all MT-3724 studies − All prior occurrences of CLS across all MT-3724 studies were grade 2 or below ● Elevated C exposure observed in last 5 of 6 subjects dosed on MT-3724 monotherapy study max − Higher than expected pharmacokinetic (beyond pharmacokinetic projections) observed in these 5 subjects − All five subjects received drug from the same single lot of MT-3724 drug product − C exposures observed in these five subjects were higher than has been observed in any other subjects or studies with MT-3724 max nd − Elevated C exposures have not been observed with 2 generation ETB programs max ● Investigation ongoing and MT-3724 studies put on partial clinical hold by the FDA on Nov 4, 2020 − No new enrollment; patients on drug and benefiting will continue to receive MT-3724; lot in question held until investigation is complete ● Other MTEM studies continue and are not affected − TAK169, MT-5111 and planned MT-6402 MOLECULAR TEMPLATES 2021 Corporate Presentation I 8

2nd-Generation ETBs Increased Potency; Better Safety; Reduced Aggregation2nd-Generation ETBs Increased Potency; Better Safety; Reduced Aggregation

nd 2 -gen ETBs Designed to Have Improved Potency and Reduced Toxicity First-gen ETB Next-gen ETBs Wildtype SLTA payload Proprietary De-immunized SLTA payload NHP Tox: HNSTD > 500 ug/kg NHP Tox: HNSTD < 150 ug/kg Treatment- experienced Therapeutic Index Therapeutic Index Treatment- 5 In-vitro potency (IC ): ~sub-nanomolar naïve 50 In-vitro potency (IC ): ~pico to sub-picomolar 50 › MT-3724 utilizes wild-type SLTA payload with intact › ETBs utilize next-gen SLTA payload de-immunized to reduce innate receptor interaction (TLR4) adaptive and innate immunogenicity › ETB structural modifications (orientation) greatly improve › Suboptimal structure orientation potency (more efficient intracellular routing) MOLECULAR TEMPLATES 2021 Corporate Presentation I 10nd 2 -gen ETBs Designed to Have Improved Potency and Reduced Toxicity First-gen ETB Next-gen ETBs Wildtype SLTA payload Proprietary De-immunized SLTA payload NHP Tox: HNSTD > 500 ug/kg NHP Tox: HNSTD < 150 ug/kg Treatment- experienced Therapeutic Index Therapeutic Index Treatment- 5 In-vitro potency (IC ): ~sub-nanomolar naïve 50 In-vitro potency (IC ): ~pico to sub-picomolar 50 › MT-3724 utilizes wild-type SLTA payload with intact › ETBs utilize next-gen SLTA payload de-immunized to reduce innate receptor interaction (TLR4) adaptive and innate immunogenicity › ETB structural modifications (orientation) greatly improve › Suboptimal structure orientation potency (more efficient intracellular routing) MOLECULAR TEMPLATES 2021 Corporate Presentation I 10

nd 2 -gen ETBs Designed to Have Reduced Propensity for Aggregation st MT-3724 (1 -Gen ETB) 2nd-Gen ETBs st- nd 1 gen ETB scaffold design exhibits propensity to form higher order 2 -Gen ETB scaffold designs prevents the creation of multiple species and aggregates via covalent and non-covalent interactions covalent aggregation ● 25-mer linker in scFv used to force monomers (MT-5111) ● 15-mer linker in scFv can create dimers and monomers ● 5-mer linker used to create diabodies (TAK-169 and MT-6402) ● Free cysteine on SLTA scaffold used to create dimers via oxidation step during purification ● No free cysteine in Next-Gen SLTA scaffold MT-3724 rd ● MT-6402, 3 -gen ETB, utilizes immunodominant 9-mer CMV peptide Free Cysteine (hydrophobic) fused to C-terminus for Antigen Seeding nd 2 gen ETBs Non-Covalent Dimer Covalent Dimer Cysteine Removed Monomer Variants HMW Aggregates TAK-169 MT-5111 Monomer Dimer Other HMW Aggregate Forms… MOLECULAR TEMPLATES 2021 Corporate Presentation I MT-3724 Heterogeneous Speciesnd 2 -gen ETBs Designed to Have Reduced Propensity for Aggregation st MT-3724 (1 -Gen ETB) 2nd-Gen ETBs st- nd 1 gen ETB scaffold design exhibits propensity to form higher order 2 -Gen ETB scaffold designs prevents the creation of multiple species and aggregates via covalent and non-covalent interactions covalent aggregation ● 25-mer linker in scFv used to force monomers (MT-5111) ● 15-mer linker in scFv can create dimers and monomers ● 5-mer linker used to create diabodies (TAK-169 and MT-6402) ● Free cysteine on SLTA scaffold used to create dimers via oxidation step during purification ● No free cysteine in Next-Gen SLTA scaffold MT-3724 rd ● MT-6402, 3 -gen ETB, utilizes immunodominant 9-mer CMV peptide Free Cysteine (hydrophobic) fused to C-terminus for Antigen Seeding nd 2 gen ETBs Non-Covalent Dimer Covalent Dimer Cysteine Removed Monomer Variants HMW Aggregates TAK-169 MT-5111 Monomer Dimer Other HMW Aggregate Forms… MOLECULAR TEMPLATES 2021 Corporate Presentation I MT-3724 Heterogeneous Species

st nd Purity (SE-UPLC): 1 -gen ETB (MT-3724) vs 2 -gen ETB (MT-5111) st MT-3724 (1 gen) scaffold exhibits propensity to form higher 2nd-gen scaffold prevents the creation of multiple order aggregates via covalent and non-covalent interactions species and covalent aggregation nd st MT-3724 (1 gen ETB) MT-5111 (2 -gen ETB) Lot AG3545 Covalent dimer: 75% Monomer: 97% Non-covalent dimer: 10% HMW: 2% HMW: 12% LMW: 1% LMW: 3% Extended HMW shoulder MOLECULAR TEMPLATES 2021 Corporate Presentation I 12st nd Purity (SE-UPLC): 1 -gen ETB (MT-3724) vs 2 -gen ETB (MT-5111) st MT-3724 (1 gen) scaffold exhibits propensity to form higher 2nd-gen scaffold prevents the creation of multiple order aggregates via covalent and non-covalent interactions species and covalent aggregation nd st MT-3724 (1 gen ETB) MT-5111 (2 -gen ETB) Lot AG3545 Covalent dimer: 75% Monomer: 97% Non-covalent dimer: 10% HMW: 2% HMW: 12% LMW: 1% LMW: 3% Extended HMW shoulder MOLECULAR TEMPLATES 2021 Corporate Presentation I 12

2nd-Generation ETBs MT-5111 / HER22nd-Generation ETBs MT-5111 / HER2

nd MT-5111: A 2 -Generation HER-Targeted ETB H E R 2 TA R G E T E D MT-5111: Single-chain variable fragment (scFv) with 2nd-Generation ETB specificity to HER2. Binds a distinct epitope from trastuzumab/pertuzumab N O V E L E N Z Y M AT I C P AY L O A D Primary mechanism of cell-kill - enzymatic ribosome destruction. pM potency against HER2 binding antibody fragment HER2+ cells S M A L L S I Z E F O R B E T T E R P E N E T R AT I O N 55 kDa versus ~145 kDa for Mabs/ADCs DI SLTA Payload O T H E R P R O P E R T I E S Fusion protein; no linker chemistry. Short serum half-life; irreversible intra-cellular effects D E I M M U N I Z E D P AY L O A D De-immunized SLTA payload for reduced innate and adaptive response. Reduced TLR4 interaction to minimize innate triggering (CLS) MOLECULAR TEMPLATES 2021 Corporate Presentation I 14nd MT-5111: A 2 -Generation HER-Targeted ETB H E R 2 TA R G E T E D MT-5111: Single-chain variable fragment (scFv) with 2nd-Generation ETB specificity to HER2. Binds a distinct epitope from trastuzumab/pertuzumab N O V E L E N Z Y M AT I C P AY L O A D Primary mechanism of cell-kill - enzymatic ribosome destruction. pM potency against HER2 binding antibody fragment HER2+ cells S M A L L S I Z E F O R B E T T E R P E N E T R AT I O N 55 kDa versus ~145 kDa for Mabs/ADCs DI SLTA Payload O T H E R P R O P E R T I E S Fusion protein; no linker chemistry. Short serum half-life; irreversible intra-cellular effects D E I M M U N I Z E D P AY L O A D De-immunized SLTA payload for reduced innate and adaptive response. Reduced TLR4 interaction to minimize innate triggering (CLS) MOLECULAR TEMPLATES 2021 Corporate Presentation I 14

MT-5111: Clinical Development When MTD reached or rec. Ph. 2 dose determined 1H21 Continued Dose Escalation Expansion in HER2+ non-MBC tumor types Cohorts of 10.0 mcg/kg and above Gastric and other HER2+ tumors in HER2+ non-MBC pts Dose Escalation Cohorts of 0.5, 1.0, 2.0, 3.0, 4.5, and 6.75 mcg/kg 1H21 (predicted tx range ≥5 mcg/kg) Expansion in MBC − Tumor types enrolled: Initial dosing at 10 mcg/kg with • MBC (n=6; all ≤3 μg/kg); biliary (n=6); pancreatic (n=2); continued dose escalation one colon and one GE junction − 1 pt w/ MBC (1 µg/kg) w/ unmeasurable disease by RECIST remained on tx for 10 cycles w/ SD, had 3 sub-cm lesions that disappeared at cycle 8 − No DLTs or cardiotoxicity have been observed to date • 6.75 mcg/kg cohort on-going MOLECULAR TEMPLATES 2021 Corporate Presentation I 15MT-5111: Clinical Development When MTD reached or rec. Ph. 2 dose determined 1H21 Continued Dose Escalation Expansion in HER2+ non-MBC tumor types Cohorts of 10.0 mcg/kg and above Gastric and other HER2+ tumors in HER2+ non-MBC pts Dose Escalation Cohorts of 0.5, 1.0, 2.0, 3.0, 4.5, and 6.75 mcg/kg 1H21 (predicted tx range ≥5 mcg/kg) Expansion in MBC − Tumor types enrolled: Initial dosing at 10 mcg/kg with • MBC (n=6; all ≤3 μg/kg); biliary (n=6); pancreatic (n=2); continued dose escalation one colon and one GE junction − 1 pt w/ MBC (1 µg/kg) w/ unmeasurable disease by RECIST remained on tx for 10 cycles w/ SD, had 3 sub-cm lesions that disappeared at cycle 8 − No DLTs or cardiotoxicity have been observed to date • 6.75 mcg/kg cohort on-going MOLECULAR TEMPLATES 2021 Corporate Presentation I 15

2nd-Generation ETBs TAK-169 / CD382nd-Generation ETBs TAK-169 / CD38

nd TAK-169: A 2 -Generation CD38-Targeted ETB C D 3 8 TA R G E T E D TAK-169: Single-chain variable fragment (scFv) with 2nd-Generation ETB specificity to CD38. Binds in the presence of daratumumab N O V E L E N Z Y M AT I C P AY L O A D Primary mechanism of cell-kill - enzymatic ribosome destruction. pM potency against CD38 binding antibody fragment CD38+ cells F O R C E D R E C E P T O R I N T E R N A L I Z AT I O N Efficient internalization against CD38, a poorly-internalizing receptor DI SLTA Payload O T H E R P R O P E R T I E S Fusion protein; no linker chemistry. Short serum half-life; irreversible intra-cellular effects D E I M M U N I Z E D P AY L O A D De-immunized SLTA payload for reduced innate and adaptive response. Reduced TLR4 interaction to minimize innate triggering (CLS) MOLECULAR TEMPLATES 2021 Corporate Presentation I 17nd TAK-169: A 2 -Generation CD38-Targeted ETB C D 3 8 TA R G E T E D TAK-169: Single-chain variable fragment (scFv) with 2nd-Generation ETB specificity to CD38. Binds in the presence of daratumumab N O V E L E N Z Y M AT I C P AY L O A D Primary mechanism of cell-kill - enzymatic ribosome destruction. pM potency against CD38 binding antibody fragment CD38+ cells F O R C E D R E C E P T O R I N T E R N A L I Z AT I O N Efficient internalization against CD38, a poorly-internalizing receptor DI SLTA Payload O T H E R P R O P E R T I E S Fusion protein; no linker chemistry. Short serum half-life; irreversible intra-cellular effects D E I M M U N I Z E D P AY L O A D De-immunized SLTA payload for reduced innate and adaptive response. Reduced TLR4 interaction to minimize innate triggering (CLS) MOLECULAR TEMPLATES 2021 Corporate Presentation I 17

nd TAK-169: 2 -Gen ETB Targeting CD38 • CD38 is a poorly-internalizing receptor central to disease CD38-targeting Agents in multiple myeloma Mab: Engineered Toxin Body: • TAK-169 efficiently internalizes and destroys low- or Darzalex TAK-169 high-expressing CD38 • TAK-169 activity is retained in the presence of daratumumab in preclinical models • TAK-169 active in patient samples (including dara- refractory) Direct cell kill Indirect CDC cell kill MOA (enzymatic ribosome • TAK-169 has shown activity in xenograph models when inactivation) dosed weekly or bi-weekly CD38 target Binding and • Reduced ADA and innate response (de-immunized Binding interaction internalization STLA scaffold) • HNSTD of 750 mcg/kg in NHPs (150 mcg/kg for MT- CD55/59 upregulation in 3724) Limitations failures, inhibiting immune None identified response • Phase I in rel/ref myeloma patients with weekly dosing started at 50 mcg/kg MOLECULAR TEMPLATES 2021 Corporate Presentation I 18nd TAK-169: 2 -Gen ETB Targeting CD38 • CD38 is a poorly-internalizing receptor central to disease CD38-targeting Agents in multiple myeloma Mab: Engineered Toxin Body: • TAK-169 efficiently internalizes and destroys low- or Darzalex TAK-169 high-expressing CD38 • TAK-169 activity is retained in the presence of daratumumab in preclinical models • TAK-169 active in patient samples (including dara- refractory) Direct cell kill Indirect CDC cell kill MOA (enzymatic ribosome • TAK-169 has shown activity in xenograph models when inactivation) dosed weekly or bi-weekly CD38 target Binding and • Reduced ADA and innate response (de-immunized Binding interaction internalization STLA scaffold) • HNSTD of 750 mcg/kg in NHPs (150 mcg/kg for MT- CD55/59 upregulation in 3724) Limitations failures, inhibiting immune None identified response • Phase I in rel/ref myeloma patients with weekly dosing started at 50 mcg/kg MOLECULAR TEMPLATES 2021 Corporate Presentation I 18

3rd-Gen ETBs / Novel Approach to IO 2nd-Gen Scaffold + antigen seeding3rd-Gen ETBs / Novel Approach to IO 2nd-Gen Scaffold + antigen seeding

rd MT-6402: PD-L1 Targeting 3 -gen ETB Direct cell-kill of PD-L1+ tumor and immune cells and alteration of the tumor CMV pp65 peptide antigen immunophenotype scFv targeting PD-L1 • ETBs localize to ER/cytosol to “seed” tumors with foreign non-self antigens De-immunized SLTA • Antigen cleaved intracellularly and presented on cell surface PD-L1 receptor in context with MHC-I CMV-specific T-cells Cleaved pp65 antigen • Delivery of pp65 CMV antigen CTL Unloaded MHC-I - Mediate native CMV-specific T cell response to tumor Cell-surface - Large existing population infected with CMV expressed PD-L1 receptor pp65/MHC-I - CMV-specific T-cells undergo “memory inflation” in response to persistent reactivation of CMV – less prone to exhaustion pp65 loaded MHC-I - Large reservoirs of CMV-specific T-cells with significant proportion specific to pp65 CMV epitope Cytokines that maintain TME PD-L1+ • Fundamental alteration of immunophenotype on tumor Tumor cell with foreign viral antigens to redirect T-cell response PD-L1+ Monocyte • FPI expected in 1H21rd MT-6402: PD-L1 Targeting 3 -gen ETB Direct cell-kill of PD-L1+ tumor and immune cells and alteration of the tumor CMV pp65 peptide antigen immunophenotype scFv targeting PD-L1 • ETBs localize to ER/cytosol to “seed” tumors with foreign non-self antigens De-immunized SLTA • Antigen cleaved intracellularly and presented on cell surface PD-L1 receptor in context with MHC-I CMV-specific T-cells Cleaved pp65 antigen • Delivery of pp65 CMV antigen CTL Unloaded MHC-I - Mediate native CMV-specific T cell response to tumor Cell-surface - Large existing population infected with CMV expressed PD-L1 receptor pp65/MHC-I - CMV-specific T-cells undergo “memory inflation” in response to persistent reactivation of CMV – less prone to exhaustion pp65 loaded MHC-I - Large reservoirs of CMV-specific T-cells with significant proportion specific to pp65 CMV epitope Cytokines that maintain TME PD-L1+ • Fundamental alteration of immunophenotype on tumor Tumor cell with foreign viral antigens to redirect T-cell response PD-L1+ Monocyte • FPI expected in 1H21

MT-6402: Potent Activity Against PD-L1+ Tumor Cells Potent effect on PD-L1+ tumor cells: Direct Cell-kill against PD-L1+ tumors through two diverse MOAs • Unprecedented alteration of tumor immunophenotype • Ribosomal destruction is independent of tumor microenvironment • Strong evidence that CMV-specific T-cells are present in tumor • Novel, potent MOA not previously used against PD-L1+ tumor types microenvironments (Rosato et al, Nature Comm 2019) MOA1 + MOA2 (AST) MOA1 (ribosomal destruction) NSCLC xenograft MOLECULAR TEMPLATES 2021 Corporate Presentation I 21 SITC 2019MT-6402: Potent Activity Against PD-L1+ Tumor Cells Potent effect on PD-L1+ tumor cells: Direct Cell-kill against PD-L1+ tumors through two diverse MOAs • Unprecedented alteration of tumor immunophenotype • Ribosomal destruction is independent of tumor microenvironment • Strong evidence that CMV-specific T-cells are present in tumor • Novel, potent MOA not previously used against PD-L1+ tumor types microenvironments (Rosato et al, Nature Comm 2019) MOA1 + MOA2 (AST) MOA1 (ribosomal destruction) NSCLC xenograft MOLECULAR TEMPLATES 2021 Corporate Presentation I 21 SITC 2019

MT-6402: Potent Activity Against PD-L1+ Immune Cells in the TME Potent effect on PD-L1+ immune cells in NHP model PD effects observed in NHP model with MT-6402 have not been seen with checkpoint antibodies A D D1 D8 D15 D22 MT-6402 depletion of Immune cells and Lymphocyte activation is associated with immune 50, 450 mcg/kg Group Dosing Immune Effects Pharmacodynamic Weekly dosing - NHP checkpoint inhibitor inflammatory signature Response MT-6402 depletes CD14+ IL-6 MT- 50 mcg/kg ↑Monocyte depletion Minimal Troponin-I B Monocytes in NHP 6402 ↑T cell, B cell, Eosinophil release; no significant IL-10 250 80 expansion increased with cardiac findings; evidence 1 sequential dosing of skin inflammation IL-4 200 IL-8 60 MT- 450 mcg/kg Troponin-I release ↑↑Monocyte depletion 6402 associated with CD3+ T ↑↑↑T cell. B cell, NK, Dose dependent 150 IFN-gamma Direct IC cell kill cardiac infiltration minimal Eosinophil expansion; Requires functional 40 TNF-alpha monocyte and B ell increased with sequential 100 SLTA 2 infiltration ; resolving with dosing IL-8 dose cessation Cytokine induction 50 20 evidence of skin IL-2, IFN-γ, TNF-α, IL-6, IL- 1 inflammation 10 0 0 50 450 450 0 SLTA- 450 mcg/kg No remarkable findings No Remarkable findings MT-6402 inactive Inactive variant Study 1: Study 2: Study 2: (mcg/kg) (mcg/kg) MT-6402 MT-6402 Inactive Variant C 450 mcg/kg 450 mcg/kg 450 mcg/kg MT-6402 expands T and B lymphocytes in NHP MT-6402 elicits a cytokine profile in NHP associated with T cell activation 1,2 – myocarditis and dermatitis are common immune-related adverse events (irAE) and responses observed with Immune Checkpoint inhibitors in the clinic 300 observed predominantly with combination immune checkpoint inhibitors in clinical settings and are associated with beneficial therapeutic response (3,4). Dose dependent PD effect 200 Immune activation (E) MT-6402 is designed to deplete PD-L1 positive IC and TC in the TME. Targeting of IC in patients has Effect of IC depletion shown clinical benefit (1,2) and combination ICI treatment can lead to immune activation and immune Not driven by blockade related adverse events (irAE) in NHP and humans correlative to favorable response (3,4). Targeting cells 100 for depletion with MT-6402 may lead to unique benefits in the clinic not observed with antibody block which mediates activity through steric block alone. (F) MT-6402 stimulates immune activation and a (A) MT-6402 or the SLTA-inactive ETB control were dosed weekly for 4 weeks in non-human pharmacodynamic and irAE profile consistent with combination but not single agent checkpoint inhibitors in primates. (B,C) Immune cell subsets were evaluated from circulation by flow cytometry. (D) 0 NHP (3,4). Reposes are dose dependent and mediated by STLA direct cell kill and not steric inhibition as the 0 50 450 450 Serum cytokine responses were evaluated across two independent studies in NHP – data is inactive control does not trigger immune activation or PD response in vivo. MT-6402 represents a unique displayed as percent of responder for study 1, n=2 NHPand study 2 n=8 NHP (MT-6402) and n=5 therapeutic approach with the ability for potent responses in humans as a single agent therapy. MT-6402 Inactive variant (inactive variant). Data reflects induction of cytokines any time after dose 3 in the studies. (mcg/kg) (mcg/kg) MOLECULAR TEMPLATES 2021 Corporate Presentation I 22 SITC 2019 Peripheral Monocyte Levels Peripheral T Lymphocyte (% of baseline) (% of baseline) % Responding - NHP dose > 3MT-6402: Potent Activity Against PD-L1+ Immune Cells in the TME Potent effect on PD-L1+ immune cells in NHP model PD effects observed in NHP model with MT-6402 have not been seen with checkpoint antibodies A D D1 D8 D15 D22 MT-6402 depletion of Immune cells and Lymphocyte activation is associated with immune 50, 450 mcg/kg Group Dosing Immune Effects Pharmacodynamic Weekly dosing - NHP checkpoint inhibitor inflammatory signature Response MT-6402 depletes CD14+ IL-6 MT- 50 mcg/kg ↑Monocyte depletion Minimal Troponin-I B Monocytes in NHP 6402 ↑T cell, B cell, Eosinophil release; no significant IL-10 250 80 expansion increased with cardiac findings; evidence 1 sequential dosing of skin inflammation IL-4 200 IL-8 60 MT- 450 mcg/kg Troponin-I release ↑↑Monocyte depletion 6402 associated with CD3+ T ↑↑↑T cell. B cell, NK, Dose dependent 150 IFN-gamma Direct IC cell kill cardiac infiltration minimal Eosinophil expansion; Requires functional 40 TNF-alpha monocyte and B ell increased with sequential 100 SLTA 2 infiltration ; resolving with dosing IL-8 dose cessation Cytokine induction 50 20 evidence of skin IL-2, IFN-γ, TNF-α, IL-6, IL- 1 inflammation 10 0 0 50 450 450 0 SLTA- 450 mcg/kg No remarkable findings No Remarkable findings MT-6402 inactive Inactive variant Study 1: Study 2: Study 2: (mcg/kg) (mcg/kg) MT-6402 MT-6402 Inactive Variant C 450 mcg/kg 450 mcg/kg 450 mcg/kg MT-6402 expands T and B lymphocytes in NHP MT-6402 elicits a cytokine profile in NHP associated with T cell activation 1,2 – myocarditis and dermatitis are common immune-related adverse events (irAE) and responses observed with Immune Checkpoint inhibitors in the clinic 300 observed predominantly with combination immune checkpoint inhibitors in clinical settings and are associated with beneficial therapeutic response (3,4). Dose dependent PD effect 200 Immune activation (E) MT-6402 is designed to deplete PD-L1 positive IC and TC in the TME. Targeting of IC in patients has Effect of IC depletion shown clinical benefit (1,2) and combination ICI treatment can lead to immune activation and immune Not driven by blockade related adverse events (irAE) in NHP and humans correlative to favorable response (3,4). Targeting cells 100 for depletion with MT-6402 may lead to unique benefits in the clinic not observed with antibody block which mediates activity through steric block alone. (F) MT-6402 stimulates immune activation and a (A) MT-6402 or the SLTA-inactive ETB control were dosed weekly for 4 weeks in non-human pharmacodynamic and irAE profile consistent with combination but not single agent checkpoint inhibitors in primates. (B,C) Immune cell subsets were evaluated from circulation by flow cytometry. (D) 0 NHP (3,4). Reposes are dose dependent and mediated by STLA direct cell kill and not steric inhibition as the 0 50 450 450 Serum cytokine responses were evaluated across two independent studies in NHP – data is inactive control does not trigger immune activation or PD response in vivo. MT-6402 represents a unique displayed as percent of responder for study 1, n=2 NHPand study 2 n=8 NHP (MT-6402) and n=5 therapeutic approach with the ability for potent responses in humans as a single agent therapy. MT-6402 Inactive variant (inactive variant). Data reflects induction of cytokines any time after dose 3 in the studies. (mcg/kg) (mcg/kg) MOLECULAR TEMPLATES 2021 Corporate Presentation I 22 SITC 2019 Peripheral Monocyte Levels Peripheral T Lymphocyte (% of baseline) (% of baseline) % Responding - NHP dose > 3

ETBs and IO: PD-L1 ETB Moving to Clinic; New IO Targets in the Works Exploration of additional IO targets where ETB Potent effect on PD-L1+ tumor cells and approach may provide substantial differentiation immune cells CTLA4 lead development work underway; IND Direct cell-kill on tumor cells through ribosomal filing expected in 2021 destruction (MOA1) independent of tumor microenvironment Potential safety and efficacy benefits around Novel alteration of cancer cell direct cell-kill of CTLA4+ T cells vs blocking immunophenotype for pre-existing, synaptic T- cell recognition of tumor (MOA2) Early in vivo and in vitro data suggest potent activity on PD-L1 immune cells and activation of immune system MOLECULAR TEMPLATES 2021 Corporate Presentation I 23ETBs and IO: PD-L1 ETB Moving to Clinic; New IO Targets in the Works Exploration of additional IO targets where ETB Potent effect on PD-L1+ tumor cells and approach may provide substantial differentiation immune cells CTLA4 lead development work underway; IND Direct cell-kill on tumor cells through ribosomal filing expected in 2021 destruction (MOA1) independent of tumor microenvironment Potential safety and efficacy benefits around Novel alteration of cancer cell direct cell-kill of CTLA4+ T cells vs blocking immunophenotype for pre-existing, synaptic T- cell recognition of tumor (MOA2) Early in vivo and in vitro data suggest potent activity on PD-L1 immune cells and activation of immune system MOLECULAR TEMPLATES 2021 Corporate Presentation I 23

Engineered Toxin Bodies A Robust Pipeline with Clinical Data in 2021Engineered Toxin Bodies A Robust Pipeline with Clinical Data in 2021

Robust Clinical Pipeline Driving Value of Drug Candidates and Platform Program (Target) Indication/Phase 1Q21 2Q21 3Q21 4Q21 Potential resolution of Decision regarding MT-3724 Ph. 2 studies MT-3724 NHL/Ph. 2 (CD20) partial clinical hold vs. acceleration of next-gen CD20 ETB Phase 1 dose escalation data update Completion of dose esc. Potential interim dose exp. data MT-5111 Solid tumors/Ph. 1 (HER2) Initiation of breast cancer exp. cohort Read on platform in solid tumor Initiation of gastric exp. cohort Potential interim dose escalation data TAK-169 Multiple myeloma/ Ph. 1 nd (CD38) Validation of de-immunized 2 -Gen scaffold MT-6402 Initiation of Ph. 1 Potential interim dose esc. data Solid tumors/Ph. 1 in 2Q (PD-L1 + AST) rd 3 -gen ETB scaffold Pipeline Preclinical data presentations Preclinical data presentations Various/Preclinical (CTLA-4, SLAMF-7, CTLA-4 ETB IND filing CD45) Takeda preclin multi-target Partnerships + (TBD) New Bus Dev Vertex preclin. multi-target (Myeloablation) MOLECULAR TEMPLATES 2021 Corporate Presentation I 25Robust Clinical Pipeline Driving Value of Drug Candidates and Platform Program (Target) Indication/Phase 1Q21 2Q21 3Q21 4Q21 Potential resolution of Decision regarding MT-3724 Ph. 2 studies MT-3724 NHL/Ph. 2 (CD20) partial clinical hold vs. acceleration of next-gen CD20 ETB Phase 1 dose escalation data update Completion of dose esc. Potential interim dose exp. data MT-5111 Solid tumors/Ph. 1 (HER2) Initiation of breast cancer exp. cohort Read on platform in solid tumor Initiation of gastric exp. cohort Potential interim dose escalation data TAK-169 Multiple myeloma/ Ph. 1 nd (CD38) Validation of de-immunized 2 -Gen scaffold MT-6402 Initiation of Ph. 1 Potential interim dose esc. data Solid tumors/Ph. 1 in 2Q (PD-L1 + AST) rd 3 -gen ETB scaffold Pipeline Preclinical data presentations Preclinical data presentations Various/Preclinical (CTLA-4, SLAMF-7, CTLA-4 ETB IND filing CD45) Takeda preclin multi-target Partnerships + (TBD) New Bus Dev Vertex preclin. multi-target (Myeloablation) MOLECULAR TEMPLATES 2021 Corporate Presentation I 25