RHOT1

Initiation of Phase 1b Study of GT-02287 in Parkinson’s patients expected by end of 2024BETHESDA, Md., Nov. 14, 2024 (GLOBE NEWSWIRE) -- Gain Therapeutics, Inc. (Nasdaq: GANX) (“Gain”, or the “Company”), a clinical-stage biotechnology company leading the discovery and development of the next generation of allosteric small molecule therapies, today reports financial results for the quarter ended September 30, 2024, and provides a corporate update. “The third quarter of 2024 marked substantial progress for Gain and the development of GT-02287, our lead candidate for the treatment of Parkinson’s disease in patients with or without the GBA1 mutation. Data from our Phase 1 study for GT-02287 presented recently at both the International Congress of Parkinson’s Disease and Movement Disorders and the Michael J Fox Foundation Annual Parkinson's Disease Therapeutics Conference demonstrated target engagement with a 53% increase in GCase activity along with favorable safety and tolerability in healthy volunteers. We believe these outcomes derisk the upcoming Phase 1b study in patients with Parkinson’s disease, which remains on track to initiate before year end 2024. We also submitted the pre-IND package for our upcoming meeting with the FDA scheduled before year end to facilitate the Phase 2 expansion of our clinical development plans for GT-02287 in 2025, moving us significantly closer to developing the first disease-modifying therapy for patients with Parkinson’s disease,” said Gene Mack, Interim CEO and CFO of Gain Therapeutics. Third Quarter 2024 and Recent Corporate Highlights Pipeline Updates Announced positive results from the Multiple Ascending Dose (MAD) part of the Phase 1 study of GT-02287, the Company’s lead candidate being evaluated for the treatment of Parkinson’s disease with or without a GBA1 mutation. Results from the study demonstrated the safety and tolerability of GT-02287 along with an increase in GCase activity of 53% in healthy volunteers. The positive results from the Phase 1 study and design of the upcoming Phase 1b clinical trial were featured at the following conferences: A late-breaker poster and oral presentation at the International Congress of Parkinson’s Disease and Movement Disorders in September 2024 in Philadelphia, PA. The poster is available here.An oral presentation at the Michael J. Fox Foundation’s 16th Annual Parkinson’s Disease Therapeutics Conference in October 2024 in New York, NY.A virtual webinar hosted by Gain Therapeutics in September 2024 that reviewed all the data from the study. A replay of the event can be accessed here. Presented preclinical data at the Neuroscience 2024 conference in October 2024 in Chicago, IL that the Company believes further elucidates the disease modifying potential of GT-02287 by evaluating the effect of withdrawing treatment in animal models and the improvement in mitochondrial health related to administration of GT-02287. GT-02287 was shown to rescue deficits in neuromuscular function and motor coordination in animal models of GBA1 and idiopathic Parkinson’s disease models and to prevent the development of deficits in cognition and activities of daily living. Notably, withdrawal of GT-02287 for more than one week did not significantly affect performance in any of the tests, suggesting a disease-modifying effect.GT-02287 reduced the level of mitochondrial reactive oxygen species (ROS) as well as ameliorating lysosomal pathology, reducing α-synuclein aggregation, and providing a neuroprotective effect. In an in vivo model in which mice were subjected to toxic insult by CBE and injection of α-synuclein preformed fibrils (PFFs) into the striatum – delayed administration of GT-02287 reduced levels of mitochondrial protein Miro1, an important maker for mitophagy; aggregated α-synuclein and plasma neurofilament light chain (NfL), a marker of neurodegeneration; as well as completely restoring motor function to control levels. Presented poster in October 2024 in Barcelona, Spain highlighting the Company’s Magellan™ drug discovery platform to identify allosteric inhibitors targeting discoidin domain receptor 2 at the 36th EORTC-NCI-AACR Symposium. Upcoming Milestones Initiation of Phase 1b trial evaluating GT-02287 in Parkinson’s disease patients expected in Q4 2024Pre-IND meeting with the U.S. Food and Drug Administration (FDA) anticipated by the end of 2024 Q3 2024 Financial Results Research and development expenses increased by $0.3 million to $2.6 million for the three months ended September 30, 2024, as compared to $2.3 million for the three months ended September 30, 2023. The increase in research and development expenses was primarily related to costs associated with the Clinical Phase 1 trial of our lead program GT-02287 for the treatment of Parkinson’s Disease. General and administrative expenses decreased by $0.7 million to $1.8 million for the three months ended September 30, 2024, as compared to $2.5 million for the three months ended September 30, 2023. The decrease in general and administrative expenses for the period was primarily attributable to a decrease in legal and professional fees relating to general corporate matters and a decrease in stock-based compensation expenses. Net loss for the three months ended September 30, 2024, was $0.17 per share, basic and diluted, compared to $0.37 per share, basic and diluted, for the three months ended September 30, 2023. Cash, cash equivalent and marketable securities were $12 million as of September 30, 2024, compared to $16.8 million as of December 31, 2023. About Gain Therapeutics, Inc.Gain Therapeutics, Inc. is a clinical-stage biotechnology company leading the discovery and development of next generation allosteric therapies. Gain’s lead drug candidate, GT-02287 is currently being evaluated for the treatment of Parkinson’s disease with or without a GBA1 mutation. Results from a Phase 1 study of GT-02287 in healthy volunteers demonstrated favorable safety and tolerability, plasma exposure in the projected therapeutic range, CNS exposure, and target engagement and modulation of GCase enzyme. Gain’s unique approach enables the discovery of novel, allosteric small molecule modulators that can restore or disrupt protein function. Deploying its highly advanced Magellan™ platform, Gain is accelerating drug discovery and unlocking novel disease-modifying treatments for untreatable or difficult-to-treat disorders including neurodegenerative diseases, rare genetic disorders and oncology. Forward-Looking StatementsThis release contains “forward-looking statements” made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements are typically preceded by words such as “believes,” “expects,” “anticipates,” “intends,” “will,” “may,” “should,” or similar expressions. These forward-looking statements reflect management’s current knowledge, assumptions, judgment and expectations regarding future performance or events. Although management believes that the expectations reflected in such statements are reasonable, they give no assurance that such expectations will prove to be correct or that those goals will be achieved, and you should be aware that actual results could differ materially from those contained in the forward-looking statements. Forward-looking statements are subject to a number of risks and uncertainties, including, but not limited to, risks associated with market conditions and the satisfaction of customary closing conditions related to the offering and uncertainties related to the offerings and the use of proceeds from the offerings. For a further description of the risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to the Company’s business in general, please refer to the Company’s prospectus supplement to be filed with the SEC, and the documents incorporated by reference therein, including the Company’s Form 10-K for the year ended December 31, 2023 and Form 10-Q for the quarter ended September 30, 2024. All forward-looking statements are expressly qualified in their entirety by this cautionary notice. You are cautioned not to place undue reliance on any forward-looking statements, which speak only as of the date of this release. We have no obligation, and expressly disclaim any obligation, to update, revise or correct any of the forward-looking statements, whether as a result of new information, future events or otherwise. Investor Contacts:Apaar Jammu and Chuck Padalaajammu@gaintherapeutics.comchuck@lifesciadvisors.com Media Contacts:Russo PartnersNic Johnson and Elio Ambrosionic.johnson@russopartnersllc.comelio.ambrosio@russopartnersllc.com(760) 846-9256 GAIN THERAPEUTICS, INC.CONDENSED CONSOLIDATED STATEMENTS OF OPERATIONS(unaudited) Three Months Ended September 30, Nine Months Ended September 30, 2024 2023 2024 2023Revenues: Collaboration revenues $— $— $— $55,180 Other income — — — — Total revenues $— $— $— $55,180 Operating expenses: Research and development (2,621,722) (2,367,482) (9,566,259) (9,146,630)General and administrative (1,837,242) (2,517,523) (7,453,229) (8,754,453)Total operating expenses (4,458,964) (4,885,005) (17,019,488) (17,901,083) Loss from operations $(4,458,964) $(4,885,005) $(17,019,488) $(17,845,903) Other income/(expense): Interest income, net 105,405 106,000 305,239 387,964 Foreign exchange gain/(loss), net (121,139) 82,198 103,362 (20,839)Loss before income tax $(4,474,698) $(4,696,807) $(16,610,887) $(17,478,778) Income tax (10,994) (21,456) (32,077) (64,773) Net loss $(4,485,692) $(4,718,263) $(16,642,964) $(17,543,551) Net loss per shares: Net loss per share attributable to common stockholders - basic and diluted $(0.17) $(0.37) $(0.78) $(1.42)Weighted average common shares - basic and diluted 26,531,747 12,701,401 21,273,422 12,342,031 GAIN THERAPEUTICS, INC.CONDENSED CONSOLIDATED BALANCE SHEETS(unaudited) September 30, December 31, 2024 2023Assets Current assets: Cash and cash equivalents $12,049,522 $11,794,949 Marketable securities - current — 4,999,704 Tax credits 373,726 242,577 Prepaid expenses and other current assets 1,318,092 741,638 Total current assets $13,741,340 $17,778,868 Non-current assets: Property and equipment, net $119,610 $125,962 Internal-use software 156,256 193,375 Operating lease - right of use assets 281,578 459,215 Restricted cash 33,873 34,021 Long-term deposits and other non-current assets 33,007 17,890 Total non-current assets 624,324 830,463 Total assets $14,365,664 $18,609,331 Liabilities and stockholders' equity Current liabilities: Accounts payable $1,098,453 $1,318,965 Operating lease liability - current 178,781 229,693 Other current liabilities 2,491,254 2,160,366 Deferred income - current 708,027 1,122,138 Loans - current 118,280 118,797 Total current liabilities $4,594,795 $4,949,959 Non-current liabilities: Defined benefit pension plan $323,266 $307,454 Operating lease liability - non-current 96,222 229,855 Deferred income - non-current 65,869 94,786 Loans - non-current 376,130 449,053 Total non-current liabilities 861,487 1,081,148 Total liabilities $5,456,282 $6,031,107 Stockholders’ equity Preferred stock, $0.0001 par value; 10,000,000 shares authorized; nil shares issued and outstanding as of September 30, 2024 and December 31, 2023. — — Common stock, $0.0001 par value: 50,000,000 shares authorized; 25,962,246 issued and outstanding as of September 30, 2024; 16,206,680 issued and outstanding as of December 31, 2023. 2,596 1,621 Additional paid-in capital 86,090,657 73,113,079 Accumulated other comprehensive income 242,810 247,241 Accumulated deficit (60,783,717) (38,516,197)Loss for the period (16,642,964) (22,267,520)Total stockholders’ equity 8,909,382 12,578,224 Total liabilities and stockholders’ equity $14,365,664 $18,609,331

GT-02287 Demonstrates Disease Modifying Capacity in Both GBA1 and Idiopathic Parkinson’s Disease Models GT-02287 Improves Mitochondrial Function and Provides Neuroprotective Effect in GBA1-Parkinson’s Disease Models GT-02287 Prevents Tau Accumulation in a Cellular Model BETHESDA, Md., Oct. 07, 2024 (GLOBE NEWSWIRE) -- Gain Therapeutics, Inc. (Nasdaq: GANX) (“Gain”, or the “Company”), a clinical-stage biotechnology company leading the discovery and development of the next generation of allosteric small molecule therapies, today announced the presentation of new evidence supporting the disease-modifying activity of GT-02287 in preclinical animal models of both GBA-1 and idiopathic Parkinson’s disease during a late-breaker poster session yesterday at the Society for Neuroscience (SfN) 2024 conference that is being held October 5-9 in Chicago, IL. In animal models of GBA-1 and idiopathic Parkinson’s disease, rescue of motor and cognitive function associated with administration of GT-02287 was observed to be persistent upon wash out of GT-02287 without significant effect in performance for more than a week following discontinuation when compared to the animals in which treatment was continued. Another presentation for GT-02287 yesterday described its association with improved mitochondrial function and neuroprotection in GBA1-Parkinson’s disease models. Finally, a second late-breaker was presented describing the reduction in Tau accumulation associated with GT-02287 in both GBA-1 mutation and wild type cell lines, suggesting GT-02287 may have broader potential as a treatment for tauopathies such as Alzheimer’s disease. “The robust preclinical development dossier for GT-02287 presented further strengthen our belief that GT-02287 has the potential to be a disease-modifying therapy for people suffering from Parkinson’s disease. The data demonstrate rescue of motor deficit and prevention of development of deficits in cognition which persisted even once the compound was removed. Moreover, GT-02287 demonstrated a positive effect on mitochondrial health as well as on lysosomal health which further demonstrates that the molecule acts throughout the disease cascade resulting from dysfunction of the lysosomal enzyme glucocerebrosidase (GCase), which GT-02287 was designed to target. Additionally, GT-02287 prevented Tau accumulation in human cellular models which demonstrates its potential to be a treatment for Alzheimer’s disease and other tauopathies,” commented Joanne Taylor, Ph.D., Senior Vice President of Research at Gain “The preservation of motor and cognitive improvement in animal models of Parkinson’s disease associated with GT-02287 after its discontinuation coupled with the neuroprotective effects after delayed administration support the potential of GT-02287 to slow or stop the progression of Parkinson’s disease,” said Gene Mack, Interim CEO and CFO of Gain Therapeutics. “The potential of GCase as a therapeutic target beyond Parkinson’s Disease is an encouraging finding that we can incorporate into our future development plans for GT-02287.” The late-breaking poster titled, “GT-02287, a clinical stage GCase regulator, demonstrates disease modifying capacity in both GBA1 and idiopathic Parkinson’s disease models,” was presented on-site October 6 at 3pm CT. In animal models of both GBA1 and idiopathic Parkinson’s disease, GT-02287 was administered after a clinical phenotype was established and then withdrawn from half the animals for more than one week prior to conclusion of the study. Neuromuscular function, motor coordination, and activities of daily living/cognition were measured in wire hang, beam walk, and nest building tests, respectively, throughout the study. GT-02287 was shown to rescue deficits in neuromuscular function and motor coordination in both models as well as to prevent the development of deficits in cognition and activities of daily living. Notably, withdrawal of GT-02287 for more than one week did not significantly affect performance in any of the tests, suggesting a disease modifying effect. The poster titled, “GT-02287, a clinical stage GCase regulator, improves mitochondrial function and provides a neuroprotective effect in GBA1-Parkinson's disease models,” was presented on-site October 6 at 10am CT. In an in vitro model - in which cultured rat mesencephalic dopaminergic neurons were treated with conduritol beta epoxide (CBE) to cause partial knockdown of GCase activity comparable to that seen in PD patients carrying heterozygous GBA1 mutations (GBA1 is the gene encoding GCase)- treatment with GT-02287 reduced the level of mitochondrial reactive oxygen species (ROS) as well as ameliorating lysosomal pathology, reducing α-synuclein aggregation, and providing a neuroprotective effect. In an in vivo model in which mice were subjected to toxic insult by CBE and injection of α-synuclein preformed fibrils (PFFs) into the striatum – delayed administration of GT-02287 reduced levels of mitochondrial protein Miro1, an important maker for mitophagy; aggregated α-synuclein and plasma neurofilament light chain (NfL), a marker of neurodegeneration; as well as completely restoring motor function to control levels. The late-breaking poster titled, “GT-02287, a GCase modulator and Gain Therapeutics’ PD drug candidate prevents Tau accumulation in a cellular model,” was presented on-site October 6 at 1pm CT. Lysosomal Tau accumulation was quantified in human fibroblasts, carrying either the L444P mutant or wild-type (WT) GBA engineered to express labelled Tau protein, at basal conditions as well in the presence of Alzheimer’s brain-derived Tau seeds. Basal and seed-induced Tau accumulation was significantly higher in Tau-GBA L444P cells, which express defective GCase, compared to Tau WT GBA cells. Treatment with GT-02287 reduced Tau accumulation in both cells carrying the L444P GBA mutation and those carrying wild-type GBA, demonstrating GT-02287’s potential as a disease-modifying treatment for Alzheimer’s disease and other tauopathies. This work was carried out in collaboration with scientists in the group of Professor Paolo Paganetti at the Laboratories for Translational Research of the Ente Ospedaliero Cantonale (LRT-EOC) in Bellinzona, Switzerland. This study was conducted under the support of an Innosuisse-Swiss Innovation Agency grant with the LRT-EOC and the Università della Svizzera italiana-affiliated Institute for Research in Biomedicine in Bellinzona, Switzerland. PDFs of the posters presented at Neuroscience 2024 are available on the Science and Technology section of the Company’s website at https://gaintherapeutics.com/science-and-technology/posters. About GT-02287Gain Therapeutics’ lead drug candidate, GT-02287, is in clinical development for the treatment of Parkinson’s disease with or without a GBA1 mutation. The orally administered, brain-penetrant small molecule is an allosteric protein modulator that restores the function of the lysosomal protein enzyme glucocerebrosidase (GCase) which becomes misfolded and impaired due to mutations in the GBA1 gene, the most common genetic abnormality associated with PD, or other age-related stress factors. In preclinical models of PD, GT-02287 restored GCase enzymatic function, reduced aggregated α-synuclein, neuroinflammation and neuronal death, increased dopamine levels and improved motor function and cognitive performance. Additionally, GT-02287 significantly reduced plasma neurofilament light chain (NfL) levels, an emerging biomarker for neurodegeneration. Compelling preclinical data in mouse models of GBA1-PD, including that presented at FENS Forum 2024 in June describing improvement in cognitive performance in addition to motor performance after administration of GT-02287, suggests that GT-02287 may have the potential to slow the progression of Parkinson’s disease. Gain’s lead program in Parkinson’s disease has been awarded funding support from The Michael J. Fox Foundation for Parkinson’s Research (MJFF) and The Silverstein Foundation for Parkinson’s with GBA, as well as from the Eurostars-2 joint program with co-funding from the European Union Horizon 2020 research and Innosuisse – Swiss Innovation Agency. About Gain Therapeutics, Inc.Gain Therapeutics, Inc. is a clinical-stage biotechnology company leading the discovery and development of next generation allosteric therapies. Gain’s lead drug candidate, GT-02287 is currently being evaluated for the treatment of Parkinson’s disease with or without a GBA1 mutation. Results from a Phase 1 study of GT-02287 in healthy volunteers demonstrated favorable safety and tolerability, plasma exposure in the projected therapeutic range, CNS exposure, and target engagement and modulation of GCase enzyme. Gain’s unique approach enables the discovery of novel, allosteric small molecule modulators that can restore or disrupt protein function. Deploying its highly advanced Magellan™ platform, Gain is accelerating drug discovery and unlocking novel disease-modifying treatments for untreatable or difficult-to-treat disorders including neurodegenerative diseases, rare genetic disorders and oncology. Forward-Looking StatementsThis release contains “forward-looking statements” made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements are typically preceded by words such as “believes,” “expects,” “anticipates,” “intends,” “will,” “may,” “should,” or similar expressions. These forward-looking statements reflect management’s current knowledge, assumptions, judgment and expectations regarding future performance or events. Although management believes that the expectations reflected in such statements are reasonable, they give no assurance that such expectations will prove to be correct or that those goals will be achieved, and you should be aware that actual results could differ materially from those contained in the forward-looking statements. Forward-looking statements are subject to a number of risks and uncertainties, including, but not limited to, risks associated with market conditions and the satisfaction of customary closing conditions related to the offering and uncertainties related to the offerings and the use of proceeds from the offerings. For a further description of the risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to the Company’s business in general, please refer to the Company’s prospectus supplement to be filed with the SEC, and the documents incorporated by reference therein, including the Company’s Form 10-K for the year ended December 31, 2023 and Form 10-Q for the quarter ended June 30, 2024. All forward-looking statements are expressly qualified in their entirety by this cautionary notice. You are cautioned not to place undue reliance on any forward-looking statements, which speak only as of the date of this release. We have no obligation, and expressly disclaim any obligation, to update, revise or correct any of the forward-looking statements, whether as a result of new information, future events or otherwise. Investor Contacts:Apaar Jammu and Chuck Padalaajammu@gaintherapeutics.comchuck@lifesciadvisors.com Media Contacts:Russo PartnersNic Johnson and Elio Ambrosionic.johnson@russopartnersllc.comelio.ambrosio@russopartnersllc.com(760) 846-9256

SAN FRANCISCO--(BUSINESS WIRE)-- Atomwise announced today results from the AIMS (Artificial Intelligence Molecular Screen) initiative that establish the AtomNet AI Platform as a viable alternative to high-throughput screening (HTS) and verify its ability to consistently discover structurally novel chemical matter. The landmark study applied AtomNet to 318 targets through collaborations with over 250 academic labs across 30 countries, representing the largest and most comprehensive virtual HTS campaign reported to date. In a paper published in Nature Scientific Reports, AtomNet successfully identified structurally novel hits for 235 of 318 targets evaluated, representing a significant improvement in hit success rate over traditional HTS. AtomNet demonstrated consistently high hit rates across all target classes, which covered a wide breadth of protein classes relevant across major therapeutic areas, confirming the broad applicability of the AI platform. AtomNet also showed a remarkable ability to discover novel chemical matter, averaging over seven structurally distinct bioactive compounds per target. Developed by Atomwise, AtomNet was the first deep neural network designed to predict the bioactivity of small molecules in structure-based drug discovery. Conventional HTS cannot evaluate over 99% of commercially available molecules, which increasingly come from synthesis-on-demand libraries. In contrast, AtomNet’s virtual HTS approach searches an expanding chemical library of more than 15 quadrillion synthesizable compounds to accurately find hits that deviate from any known binders, enabling rapid discovery from vast, unexplored chemical space. “We need new technologies for new targets. As the pharma industry increasingly moves to tackle harder and harder disease biology, we need new molecules that can address these challenges,” said Mike Varney, former Executive Vice President and Head of Genentech Research and Early Development, and Atomwise Board Member. “For a generation, the pharma industry has largely relied on a single source – HTS – to identify new bioactive compounds. Any new approach needs to demonstrate applicability and robustness across the entire proteome. It is exciting to see Atomwise demonstrate their successes on such a broad range of disease targets.” “The ability of AtomNet to consistently identify novel bioactive chemical compounds solves a fundamental challenge and inefficiency with current small molecule drug discovery,” said Gavin Hirst, Chief Scientific Officer of Atomwise. “Medicinal chemists always want new scaffolds to work on. A new scaffold lets you make progress and potentially unlocks different selectivity, pharmacokinetics, or pharmacodynamics. Access to new scaffolds increases the probability that the developed molecule will meaningfully differentiate in the clinic.” For most projects, the AtomNet training data contained no active molecules for the target protein or any close homologs. As a result, discovered hits often represent first-in-class binders for newly discovered or difficult-to-target proteins. Examples from the AIMS initiative include the first reducer for Miro1, a new target in Parkinson’s disease, the first inhibitors for OTUD7A and OTUD7B, challenging deubiquitinase targets for solid and hematological tumors, and small molecule inhibitors for CTLA-4, a well-established oncology target. “Generally the predictive power of virtual screening platforms has been extremely limited,” said Prof. Gregory Bowman of the University of Pennsylvania, who used AtomNet to uncover a cryptic site for phosphatase PPM1D, a therapeutic target in oncology. “Results of the AIMS study show that AtomNet has a high success rate in finding hits for traditionally challenging biology, like allosteric or protein-protein interactions. This noteworthy ability opens the door for many targets that have been previously deemed intractable.” “AtomNet enabled us to discover highly selective inhibitors for two emerging targets with potential applicability across a range of cancers, but lacking known non-covalent binders,” said Pengda Liu, Ph.D., assistant professor in the Department of Biochemistry and Biophysics at UNC-Chapel Hill. “Despite the novelty and challenge of these targets, the compounds AtomNet predicted are potent to the point where we are currently moving forward with medicinal chemistry efforts. It is clear that AI approaches like AtomNet can fundamentally change the way we think about what is possible, and I have no doubt that it will play a critical role in future drug development.” “We designed AtomNet to be able to extrapolate molecular learnings across targets and actively predict activity for new and challenging targets,” said Abraham Heifets, CEO, Atomwise. “Historically, one of the major challenges for AI-driven discovery has been a need for pre-existing, on-target ligand data to accurately predict activity, narrowing AI’s applicability. We’ve shown for the first time that AtomNet does not require any target-specific training data and can be applied to virtually any target, even those that have been considered undruggable.” “Comprehensively testing the capabilities of AtomNet across such a wide range of targets clearly demonstrates the unprecedented accuracy of the platform to identify novel drug-like scaffolds,” says Izhar Wallach, who led the AIMS initiative and is Chief Technology Officer of Atomwise. “We are hugely thankful for the hundreds of talented researchers across the world who made this collaboration possible.” Atomwise plans to IND application this year for its lead candidate, a novel allosteric TYK2 inhibitor with first-in-class and best-in-class potential, which was discovered using AtomNet. The company’s vision is to invent a better way to discover and develop new medicines to help patients. Our belief is structurally novel chemical matter increases the likelihood of developing first-in-class and best-in-class medicines that have the potential to transform patient care. About Atomwise Atomwise is a TechBio company leveraging AI/ML to revolutionize small molecule drug discovery. The Atomwise team invented the use of deep learning for structure-based drug design, a core technology of Atomwise’s best-in-class AI discovery and optimization engine, which is differentiated by its ability to find and optimize novel chemical matter. Atomwise has extensively verified its discovery engine, having demonstrated the ability to find compounds with therapeutic potential hundreds of times across a wide variety of protein types and multiple “hard to drug” targets. Atomwise is advancing a proprietary pipeline of small-molecule drug candidates. Our vision is to invent a better way to discover and develop new medicines to help patients. Learn more at atomwise.com or follow @AtomwiseInc.