Cautionary Note on Forward-Looking Statements This presentation contains forward-looking statements. All statements other than statements of historical facts contained in this presentation, such as statements regarding o

Ascendis Pharma A/S Oncology Program

Update May 31, 2023 Exhibit 99.1

Cautionary Note on Forward-Looking

Statements This presentation contains forward-looking statements. All statements other than statements of historical facts contained in this presentation, such as statements regarding our prospective product candidates; clinical trial results; the

expected timing of future clinical trial results; the scope, progress, results and costs of developing our product candidates or any other future product candidates; timing and likelihood of success; plans and objectives of management for future

operations; and future results of current and anticipated products and product candidates are forward-looking statements. These forward-looking statements are based on our current expectations and beliefs, as well as assumptions concerning future

events. These statements involve known and unknown risks, uncertainties and other factors that could cause our actual results to differ materially from the results discussed in the forward-looking statements. These risks, uncertainties and other

factors are more fully described in our reports filed with or submitted to the Securities and Exchange Commission, including, without limitation, our most recent Annual Report on Form 20-F filed with the SEC on February 16, 2023 particularly in the

sections titled "Risk Factors" and "Operating and Financial Review and Prospects." In light of the significant uncertainties in our forward-looking statements, you should not place undue reliance on these statements or regard

these statements as a representation or warranty by us or any other person that we will achieve our objectives and plans in any specified timeframe, or at all. Any forward-looking statement made by us in this presentation speaks only as of the date

of this presentation and represents our estimates and assumptions only as of the date of this presentation. Except as required by law, we assume no obligation to update these statements publicly, whether as a result of new information, future

events, changed circumstances or otherwise after the date of this presentation. This presentation concerns product candidates that are or have been under clinical investigation and which have not yet been approved for marketing by the U.S. Food and

Drug Administration, European Medicines Agency or other foreign regulatory authorities. These product candidates are currently limited by U.S. Federal law to investigational use, and no representations are made as to their safety or effectiveness

for the purposes for which they are being investigated. Ascendis, Ascendis Pharma, the Ascendis Pharma logo, the company logo, TransCon, and SKYTROFA are trademarks owned by the Ascendis Pharma group. May 2023 Ascendis Pharma A/S. .

Oncology R&D Day Agenda Welcome

& Agenda Overview Scott T. Smith, EVP, CFO Vision 3x3 Jan M ller Mikkelsen, President & CEO TransCon Platform & Product Innovation Kennett Sprog e, Ph.D. EVP, Head of Innovation and Research 10:05-10:20 a.m. 10:00 a.m.

10:20-10:35 a.m. Clinical Development Strategy & Clinical Updates Stina Singel, M.D., Ph.D. EVP, Head of Clinical Development, Oncology Investigator Perspectives Diwakar Davar, M.D. Associate Professor; Clinical Director of Melanoma & Skin

Cancer Program, University of Pittsburgh Medical Center (UPMC), Hillman Cancer Center 11:10-11:30 a.m. 10:35-11:10 a.m. 11:30-12:00 p.m. Closing Remarks Jan M ller Mikkelsen, President & CEO Q&A Moderated by Scott T. Smith, EVP, CFO

Vision 3x3 Our Vision for Oncology Jan

Mikkelsen President & Chief Executive Officer

Vision 3x3: Building a Leading Global

Biopharma Company Our goal is to achieve sustainable growth through multiple approaches Obtain regulatory approval for three independent Endocrinology Rare Disease products TransCon hGH for pediatric growth hormone deficiency TransCon PTH for adult

hypoparathyroidism TransCon CNP for achondroplasia Grow Endocrinology Rare Disease pipeline through Global clinical reach Pursuing 9 total indications, label optimization, and life cycle management New endocrinology products Establish global

commercial presence for our Endocrinology Rare Disease area Build integrated commercial organization in North America and select European countries Establish global commercial presence through partners with local expertise and infrastructure Advance

a high-value oncology pipeline with one IND or similar filing each year Create a third independent therapeutic area with a diversified pipeline Ascendis Pharma's 2020 - 2025 strategic roadmap

Why Oncology? Very large unmet medical

need Large number of clinically validated pathways which are limited by toxicity, efficacy, and ease of administration Suitable for use with the TransCon Technology platform Systemic delivery Localized delivery Potential to address all the aspect of

the cancer immunity cycle Opportunity to expand pipeline to impact multiple aspects of anti-tumor response

Interleukin 2 Overview First

immunologic compound in cancer FDA approved for the treatment of metastatic renal cell carcinoma (1992) FDA approved for the treatment for metastatic melanoma (1998) Interleukin shown to be effective in approximately 15% of patients Number of

Responding Patients (response rate) Median Response Duration in Months (range) CR's 17 (7%) 80+* (7 to 131+) PR's 20 (8%) 20 (3 to 126+) PR's + CR's 37 (15%) 54 (3 to 131+) Clinical response data - Metastatic renal cell

carcinoma Number of Responding Patients (response rate) Median Response Duration in Months (range) CR's 17 (6%) 59+* (3 to 122+) PR's 26 (10%) 6 (1 to 111+) PR's + CR's 43 (16%) 9 (1 to 122+) Clinical response data -

Metastatic melanoma Proleukin (aldesleukin) product label (+) sign means ongoing * Median duration not yet observed; a conservative value is presented which represents the minimum median duration of response.

TransCon Technology Platform

& Product Innovation in Oncology Kennett Sprog e, Ph.D. EVP, Head of Innovation and Research

TransCon platform is uniquely suited

for amplified and durable immune activation, with the aim for addressing significant unmet medical need TransCon: An Innovative Technology Platform TransCon technologies combine the benefits of prodrug and predictable release technologies. TransCon

soluble prodrug technology validated within endocrinology with a high success rate in multiple clinical programs; SKYTROFA approved in the EU and US. TransCon hydrogel technology applied as a long-acting intratumoral (IT) delivery

platform of small molecules, peptides, proteins, antibody fragments and antibodies. TransCon IL-2 b/g is using same soluble prodrug technology as SKYTROFA, enabling sustained released of potent non-alpha IL-2. TransCon TLR7/8 Agonist is using

our hydrogel technology for sustained intratumoral immune activation, with minimal systemic exposure.

Transient Conjugation: A Powerful,

Flexible Platform Aromatic Cyclic Imide DKP Carbamate Bicin AEG Pyroglutamate Parent Drug TransCon Carrier TransCon Platform: 3 components TransCon Linker Antibodies, Antibody Fragments, Proteins, Peptides and Small Molecules Soluble Carriers

Insoluble Carriers Local TransCon TLR7/8 Agonist Systemic TransCon IL-2 / Leveraging the breath of TransCon platform to design pipeline of immuno-oncology drugs

Stimulating Local Immunity to

Achieve Systemic Effect TransCon IL-2 b/g and TransCon TLR7/8 Agonist have been designed mechanistically for monotherapy and synergistic combination effects TransCon TLR7/8 Agonist for long-acting IT delivery Turns the tumor hot Enhances education

of T cells Recruits systemic cytotoxic immune cells APC: Antigen presenting cell, TRM: Resident memory T cell, CTL: Cytotoxic T cell, NK: Natural killer cell TransCon IL-2 b/g for long-acting systemic delivery Expands & activates CD8+ T and NK

cell population Activates tumor resident effector cells locally Innate immune stimulator Adaptive immune stimulator

The Immune System in Normal Compared

to Inflamed Tissue Tissue resident immune cells survey all organs and act as first responders in response to threats Local chemokines attract effector cells from blood and surrounding tissue Local cytokines such as IL-2 proliferate, activate and

potentiate the immune response Tcirc: Circulating T cells, NK: Natural killer cells, APC: Antigen presenting cell, TRM: Tissue resident T cell (effector & memory), CTL: Cytotoxic T cell (CD8+), Tmem: Memory T cell (CD4+), Th1: T helper 1 cell,

M1: M1 macrophage Normal tissue Inflamed tissue

The Immune System in Cold versus Hot

Tumors Tcirc: Circulating T cells, NK: Natural killer cells, APC: Antigen presenting cell, TRM: Tissue resident T cell (effector & memory), CTL: Cytotoxic T cell (CD8+), Tmem: Memory T cell (CD4+), Th1 & Th2: T helper 1 or 2 cell, M1 &

M2: M1- or M2-like macrophage Innate activators like TLR7/8 Agonist can turn a cold tumor hot In cold tumors, there is no inflammation and no recruitment of effector cells In hot tumors, the tissue resident immune cells fight the cancer and may

recruit effector cells from circulation Cold tumors Hot tumor

Optimal Product Design Parameters

Ideal TLR agonist Design Sustained high local concentration Potent pro-inflammatory TLR agonist Pharmacology / PD Sustained inflammation in the tumor, with high cyto- and chemokine release Convenient dosing Clinical Clinical activity in injected and

non-injected tumor (abscopal) Well-tolerated systemic AE profile Ideal IL-2 agonist Design Long systemic half-life with low Cmax IL-2 biased to b/g with high potency and similar size to native IL-2 Pharmacology / PD Expansion of CD8+ T and NK cells,

with no expansion of EOS and Tregs Convenient dosing Clinical Broad clinical activity Well-tolerated (no grade 3/4 CRS, VLS) Administered as outpatient Innate immune system Adaptive immune system TLR: Toll-like receptor; Treg: regulatory T

cells; EOS: eosinophils; ALC absolute lymphocytes count (blood); CRS: cytokine release syndrome; VLS: vascular leak syndrome

TransCon TLR7/8 Agonist: Using

TransCon Hydrogel Technology for Targeted Intratumoral Exposure TransCon TLR7/8 Agonist

pH and temperature dependent linker

cleavage Local depot of drug loaded TransCon hydrogel carrier Sustained Local Intratumoral Release of Resiquimod Using TransCon hydrogel enables high local concentration of resiquimod with low systemic exposure

TransCon TLR7/8 Agonist: Turning the

Tumor Hot TransCon TLR7/8 Agonist is designed for high intratumoral exposure over several weeks with minimal systemic exposure and to turn the tumor hot using a potent TLR agonist1 Local and abscopal effect expected via increased antigen

presentation in tumor & draining lymph nodes2 TransCon TLR7/8 Agonist is designed to activate the antigen presenting cells locally and make tumors hot regardless of immune status Increase antigen presentation Production of chemokines Increase

intratumoral proinflammatory cytokines CXCL-10 creates homing of Teff and NK cells from tissue and blood. 1 Cellular Immunology 243 (2006) 48-57 2 Cancer Cell International (2022) 22:286

TransCon IL-2 b/g: Sustained Release

of Non-alpha IL-2 Using Validated Prodrug Technology TransCon IL-2 b/g

TransCon IL-2 b/g Best-in-Class

Design Rosen D, et al. AACR annual meeting. 2020; Poster 4507. TransCon linker slowly releases IL-2 b/g TransCon carrier IL-2 b/g TransCon linker TransCon IL-2 b/g (Prodrug) Active IL-2 b/g % Release of IL-2 b/g TransCon IL-2 b/g in vitro release

kinetics TransCon IL-2 b/g is designed to provide sustained expansion of circulating CD8+ T and NK cells. Released IL-2 b/g can distribute to tumor tissue to active resident immune cells. pH and temperature dependent linker cleavage

TransCon IL-2 / : Built

on 30 Years of Learnings TransCon IL-2 b/g is designed to enhance both local and systemic immune responses and synergize with hot tumor biology 1Data on file 2Bioconjugate Chem. 2004, 15, 6, 1304-1313 Variant / Bias Potency

reduction1 Size2 (Radius) IL-2 No n/a 2 nm IL-2 / 5 kDa Yes ~4-fold 3 nm IL-2 / 10 kDa Yes ~6-fold 4 nm IL-2 / 30 kDa Yes ~20-fold 6 nm Selectively expand reservoir of cytotoxic T- and NK cells over Tregs Low

Cmax, of released biased IL-2 / molecule, retaining native-like size Locally activate tissue-resident cytotoxic T-cells Designed for desired receptor binding, potency, and exposure / bias obtained with small 5 kDa PEG,

retaining native-like size and high potency to preferentially expand and activate cytotoxic T- and NK cells over Tregs Long half-life prodrug and low Cmax widen therapeutic index to deliver tolerable and sustained expansion of effector

Two Products Designed for

Monotherapy Effects and Synergistic Mode of Action Tcirc: Circulating T cells, NK: Natural killer cells, APC: Antigen presenting cell, TRM: Tissue resident T cell (effector & memory), CTL: Cytotoxic T cell (CD8+), Tmem: Memory T cell (CD4+),

Th1: T helper 1 cell, M1: M1 macrophage TransCon IL-2 b/g designed to robustly expand and activate immune effector cells in tumor and circulation TransCon TLR7/8 Agonist designed to increase tumor recognition for local and systemic tumor

Optimal Product Design Parameters

Ideal TLR agonist Design Sustained high local concentration Potent pro-inflammatory TLR agonist Pharmacology / PD Sustained inflammation in the tumor, with high cyto- and chemokine release Convenient dosing Clinical Clinical activity in injected and

non-injected tumor (abscopal) Well-tolerated systemic AE profile Ideal IL-2 agonist Design Long systemic half-life with low Cmax IL-2 biased to b/g with high potency and similar size to native IL-2 Pharmacology / PD Expansion of CD8+ T and NK cells,

with no expansion of EOS and Tregs Convenient dosing Clinical Broad clinical activity Well-tolerated (no grade 3/4 CRS, VLS) Administered as outpatient Innate immune system Adaptive immune system TLR: Toll-like receptor; Treg: regulatory T

cells; EOS: eosinophils; ALC absolute lymphocytes count (blood); CRS: cytokine release syndrome; VLS: vascular leak syndrome

Clinical Development Strategy &

Clinical Updates Stina Singel, M.D., Ph.D. EVP, Head of Clinical Development, Oncology

Removing the Immune Brakes Is Not

Sufficient for Majority of Tumors Hirsch et al. 2019 British Journal of Cancer 120:3-5, Reproduced with permission from Springer Nature Primary and acquired resistance to immune checkpoint inhibitors limit the benefit from checkpoint

inhibitors Response rate (ORR) of checkpoint inhibitors (CPIs) % Reprinted from Cancer Cell 37:443-455, Schoenfeld and Hellmann, 2020, with permission from Elsevier Copyrighted Image Copyrighted Image

Melanoma is the First Solid Tumor to

Demonstrate Benefit from Checkpoint Inhibitors Reprinted from Eur J Cancer, Vol /edition number, Ugurel et al., Survival of patients with advanced metastatic melanoma: The impact of MAP kinase pathway inhibition and immune checkpoint inhibition -

Update 2019, 2020; 130:126-138, with permission from Elsevier. Checkpoint inhibitors and targeted therapies have made significant impact on melanoma survival Copyrighted Image

Many Patients Do Not Benefit

Sufficiently from Checkpoint Inhibitors in Melanoma Adapted from Ugurel et al. Eur J Cancer 2020; 130:126-138 Unmet Need Anti-CTLA4 + anti-PD-1 Anti-PD-1 Anti-CTLA4

Novel Approaches Are Needed in

Melanoma Checkpoint inhibition is not sufficient here Adapted from Ugurel et al. Eur J Cancer 2020; 130:126-138 Unmet Need Anti-CTLA4 + anti-PD-1 Anti-PD-1 Anti-CTLA4

Product Candidates in Oncology

TransCon TLR7/8 Agonist