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Last update 08 May 2025

STING

Last update 08 May 2025

Basic Info

Synonyms

endoplasmic reticulum IFN stimulator, Endoplasmic reticulum interferon stimulator, ERIS

+ [14]

Introduction

Facilitator of innate immune signaling that acts as a sensor of cytosolic DNA from bacteria and viruses and promotes the production of type I interferon (IFN-alpha and IFN-beta) (PubMed:18724357, PubMed:18818105, PubMed:19433799, PubMed:19776740, PubMed:23027953, PubMed:23747010, PubMed:23910378, PubMed:27801882, PubMed:29973723, PubMed:30842659, PubMed:35045565, PubMed:35388221, PubMed:36808561, PubMed:37832545, PubMed:25704810, PubMed:39255680). Innate immune response is triggered in response to non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm (PubMed:26300263). Acts by binding cyclic dinucleotides: recognizes and binds cyclic di-GMP (c-di-GMP), a second messenger produced by bacteria, cyclic UMP-AMP (2',3'-cUAMP), and cyclic GMP-AMP (cGAMP), a messenger produced by CGAS in response to DNA virus in the cytosol (PubMed:21947006, PubMed:23258412, PubMed:23707065, PubMed:23722158, PubMed:23747010, PubMed:23910378, PubMed:26229117, PubMed:30842659, PubMed:35388221, PubMed:37379839). Upon binding to c-di-GMP, cUAMP or cGAMP, STING1 oligomerizes, translocates from the endoplasmic reticulum and is phosphorylated by TBK1 on the pLxIS motif, leading to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent anti-viral state (PubMed:22394562, PubMed:25636800, PubMed:29973723, PubMed:30842653, PubMed:35045565, PubMed:35388221). Exhibits 2',3' phosphodiester linkage-specific ligand recognition: can bind both 2'-3' linked cGAMP (2'-3'-cGAMP) and 3'-3' linked cGAMP but is preferentially activated by 2'-3' linked cGAMP (PubMed:23747010, PubMed:23910378, PubMed:26300263). The preference for 2'-3'-cGAMP, compared to other linkage isomers is probably due to the ligand itself, whichs adopts an organized free-ligand conformation that resembles the STING1-bound conformation and pays low energy costs in changing into the active conformation (PubMed:26150511). In addition to promote the production of type I interferons, plays a direct role in autophagy (PubMed:30568238, PubMed:30842662). Following cGAMP-binding, STING1 buds from the endoplasmic reticulum into COPII vesicles, which then form the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) (PubMed:30842662). The ERGIC serves as the membrane source for WIPI2 recruitment and LC3 lipidation, leading to formation of autophagosomes that target cytosolic DNA or DNA viruses for degradation by the lysosome (PubMed:30842662). Promotes autophagy by acting as a proton channel that directs proton efflux from the Golgi to facilitate MAP1LC3B/LC3B lipidation (PubMed:37535724). The autophagy- and interferon-inducing activities can be uncoupled and autophagy induction is independent of TBK1 phosphorylation (PubMed:30568238, PubMed:30842662). Autophagy is also triggered upon infection by bacteria: following c-di-GMP-binding, which is produced by live Gram-positive bacteria, promotes reticulophagy (By similarity). May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons (PubMed:18724357). May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II) (By similarity). (Microbial infection) Antiviral activity is antagonized by oncoproteins, such as papillomavirus (HPV) protein E7 and adenovirus early E1A protein (PubMed:26405230). Such oncoproteins prevent the ability to sense cytosolic DNA (PubMed:26405230).

190

Drugs associated with STING

TAK-676

Target

STING

Mechanism

STING agonists

Active Org.

Spera Pharma, Inc.

[+3]

Originator Org.

Takeda Development Center Americas, Inc.

Active Indication

Solid tumor [+5]

Inactive Indication-

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

SB-11285

Target

STING

Mechanism

STING agonists

Active Org.

F-Star Delta Ltd. [+1]

Originator Org.

F-Star Therapeutics, Inc. (United States)

Active Indication

Advanced Malignant Solid Neoplasm [+2]

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

TSN-222

Target

P4HB x STING

Mechanism

P4HB inhibitors [+1]

Active Org.

Taili Biotechnology Shanghai Co Ltd.

Originator Org.

Taili Biotechnology Shanghai Co Ltd.

Active Indication

Locally Advanced Melanoma [+3]

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with STING

NCT06601296

/ RecruitingPhase 2IIT

STING Agonist and Personalized Ultra-fractionated Stereotactic Adaptive Radiotherapy in Combination With Checkpoint Inhibition for Patients With Metastatic Kidney Cancer (SPARK)

To evaluate progression of metastatic renal cell carcinoma from the initiation of PULSAR radiotherapy in combination with IMSA101 injectable onward.

Start Date01 Apr 2025

Sponsor / Collaborator

The University of Texas Southwestern Medical Center

NCT06626633

/ RecruitingPhase 1IIT

Phase 1 Clinical Trial of the STING Agonist CRD3874-SI in Patients with Relapsed/refractory Acute Myeloid Leukemia

This clinical research study is being done to answer questions about how to treat cancer.
To clear cancer cells from the body, the immune system needs the action of proteins called Type 1 interferons. The protein STING (for STimulator of INterferon Genes) stimulates the body to make Type 1 interferons. Type 1 interferons activate key molecules in cancer immunity to kill cancer cells.
CRD3874 is a synthetic drug that activates STING, and STING stimulates the immune system to kill cancer cells. In experiments on blood from humans, CRD3874 makes blood cells produce molecules responsible for anti-cancer activity. CRD3874 was tested in mice with cancers including leukemia, head and neck cancer, lung cancer, pancreatic cancer and sarcoma. In these mice, CRD3874 made tumors shrink or disappear, and some mice developed long-lasting immunity against cancer. Also, when CRD3874 was given with other anti-cancer treatments, it increased their anti-cancer effects.

Start Date26 Aug 2024

Sponsor / Collaborator

University of Maryland Baltimore

NCT06544642

/ RecruitingPhase 1

A Phase 1 Combined Single and Multiple Ascending Oral Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics, Food Effect and Biomarker Response of ASP5502 in Healthy Adults and Participants With Primary Sjögren's Syndrome

Primary Sjögren's syndrome (pSS) is a condition when the body's immune system attacks glands that produce fluids, such as the tear and saliva glands. This leads to dry eyes and a dry mouth. However, other symptoms may occur such as fatigue, joint pain, and skin problems. These symptoms can be severe. Symptoms can be treated but there is an unmet need to treat the actual condition.
In this study, ASP5502 is being given to humans for the first time. The people taking part are healthy adults or adults with pSS. The main aims of the study are to check the safety of ASP5502 and how people tolerate ASP5502.
This study will be in 3 parts. In Part 1, healthy men and women will take tablets of ASP5502 or a placebo just once. In this study, the placebo looks like the ASP5502 tablet but doesn't have any medicine in it. Different small groups of people will take a lower to a higher dose of ASP5502 or a placebo. This will happen one group after another. One small group will take tablets of ASP5502 or placebo with and without food. This is to find out if food affects how the body processes ASP5502.
After their dose, people will stay in the medical center for a few nights. This is to have blood tests, electrocardiograms (ECGs) to check heart health, and other safety checks, and to report any medical problems. One of these checks is to have their heart continuously tracked during the first night. This is called telemetry. People who take tablets of ASP5502 or placebo with and without food will stay in the medical center for a few extra nights.
In Part 2, healthy men and women will take tablets of ASP5502 or a placebo. They will do this once a day for 2 weeks (14 days). Different small groups of people will take a lower to a higher dose of ASP5502 or a placebo. This will happen one group after another.
After taking ASP5502 or the placebo, people will stay in the medical center for a few nights. This is to have blood tests, ECGs to check heart health, and other safety checks, and to report any medical problems. Telemetry will also be done continuously during the first night.
In Part 3, men and women with pSS will take tablets of ASP5502. They will do this once a day for 4 weeks (28 days). Different small groups of people will take a lower to a higher dose of ASP5502. This will either happen for one group after another, or just for 1 group. The number of groups and the doses taken will be worked out from the results from Part 1 and Part 2 of this study. People will stay in the medical center for a couple of nights. This will happen for their first dose, then again after about 2 weeks and 4 weeks of treatment. As in Parts 1 and 2, this is to have blood tests, ECGs to check heart health, and other safety checks, and to report any medical problems.
In all parts of the study, people will return to the medical center about 1 week after their final blood sample is taken, for health check. People in parts 2 and 3 will also receive a telephone call safety check about 4 weeks after their last dose of ASP5502.

Start Date21 Aug 2024

Sponsor / Collaborator

Astellas Pharma Global Development, Inc.

100 Clinical Results associated with STING

100 Translational Medicine associated with STING

0 Patents (Medical) associated with STING

6,035

Literatures (Medical) associated with STING

31 Dec 2025·Emerging Microbes & Infections

Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2

Article

Author: Cheung, Pak-Hin Hinson ; Zhao, Wenlong ; Sun, Xiao-Yu ; Ye, Zi-Wei ; Ong, Chon-Phin ; Jin, Dong-Yan ; Chan, Pearl

Mpox virus (MPXV) has to establish efficient interferon (IFN) antagonism for effective replication. MPXV-encoded IFN antagonists have not been fully elucidated. In this study, the IFN antagonism of poxin-schlafen (PoxS) fusion gene of MPXV was characterized. MPXV PoxS was capable of decreasing cGAS-produced 2'3'-cGAMP, like its ortholog poxin of vaccinia virus, which is the first known cytosolic nuclease that hydrolyses the 3'-5' bond of 2'3'-cyclic GMP-AMP (cGAMP). However, MPXV PoxS did not suppress cGAS-STING-mediated type I IFN production. Instead, MPXV PoxS antagonized basal and type I IFN-induced expression of IFN-stimulated genes such as OAS1, SAMD9, SAMD9L, ISG15, ISG56 and IFIT3. Consistently, MPXV PoxS inhibited both basal and type I IFN-stimulated activity of interferon-stimulated response elements, but did not affect activation of IFN-γ-activated sites. Mechanistically, MPXV PoxS interacted with STAT2 and sequestered it in the cytoplasm. Both the viral schlafen fusion and the active site of 2'3'-cGAMP nuclease were required for STAT2 sequestration and consequent suppression of IFN-stimulated gene expression. MPXV PoxS conferred resistance to the suppression of MPXV replication by type I IFN. Taken together, our findings suggested that MPXV PoxS counteracts host antiviral response by sequestering STAT2 to circumvent basal and type I IFN-induced expression of antiviral genes.

31 Dec 2025·OncoImmunology

Patient-derived tumor explant models of tumor immune microenvironment reveal distinct and reproducible immunotherapy responses

Article

Author: Rannikko, Jenna H ; Koskivuo, Ilkka ; Järvinen, Petrus ; Peltonen, Karita ; Nicorici, Daniel ; Mattson, Johanna ; Tornberg, Sara ; Mustjoki, Satu ; Klefström, Juha ; Järvinen, Riikka ; Kumari, Anita N ; Turpin, Rita ; Thotakura, Anil ; Mutka, Minna ; Lahdensuo, Kanerva ; Lee, Moon Hee ; Mirtti, Tuomas ; Pouwels, Jeroen ; Liu, Ruixian ; Hollmén, Maija ; Niinikoski, Laura ; Kovanen, Panu E ; Meretoja, Tuomo ; Boström, Pia

Tumor-resident immune cells play a crucial role in eliciting anti-tumor immunity and immunomodulatory drug responses, yet these functions have been difficult to study without tractable models of the tumor immune microenvironment (TIME). Patient-derived ex vivo models contain authentic resident immune cells and therefore, could provide new mechanistic insights into how the TIME responds to tumor or immune cell-directed therapies. Here, we assessed the reproducibility and robustness of immunomodulatory drug responses across two different ex vivo models of breast cancer TIME and one of renal cell carcinoma. These independently developed TIME models were treated with a panel of clinically relevant immunomodulators, revealing remarkably similar changes in gene expression and cytokine profiles among the three models in response to T cell activation and STING-agonism, while still preserving individual patient-specific response patterns. Moreover, we found two common core signatures of adaptive or innate immune responses present across all three models and both types of cancer, potentially serving as benchmarks for drug-induced immune activation in ex vivo models of the TIME. The robust reproducibility of immunomodulatory drug responses observed across diverse ex vivo models of the TIME underscores the significance of human patient-derived models in elucidating the complexities of anti-tumor immunity and therapeutic interventions.

01 Dec 2025·Immunogenetics

Suppressed activation of the IRF7 and TLR9 by JAK2V617F gold nanoparticles

Article

Author: Sözer, Selçuk ; Demirtaş, Esra Nur ; Tokcan, Berkay

AbstractPhiladelphia chromosome-negative myeloproliferative neoplasms (Ph-MPNs) are characterized by the overproduction of myeloid cells and a lack of response to cytokine signaling, along with genomic instability and the accumulation of nucleic acids in the cytoplasm. In this study, we investigated the effects of oligonucleotide-gold nanoparticle conjugates (ON-GNPs) targeting JAK2 or JAK2V617F mRNAs on nucleic acid-sensing pathways in HEL, SET2, and K562 cell lines. We evaluated changes in gene expression related to TLR9 and cGAS/STING pathways, RAGE/TLR9 receptor dynamics, and inflammatory cytokine release over short-term (0.5–2 h) and long-term (24–72 h) exposures. Our results demonstrated that ON-GNPs transiently suppressed TLR9, IRF7, and NFKB1 expression during the short term, followed by significant upregulation after 24 h, persisting up to 72 h. Notably, JAK2V617F-targeting ON-GNPs induced heightened IRF7 activation in HEL and SET2 cells after 24 h without affecting TLR9/RAGE expression. Additionally, IL-8 secretion increased in HEL and SET2 culture media after 72 h, correlating with interferon pathway activation. This study reveals that complementary ON-GNPs can modulate nucleic acid-sensing pathways, suppressing IL-8 and inflammatory signaling in the short term while inducing delayed activation of TLR9 and IRF7 in the presence of JAK2V617F. These findings provide a promising foundation for developing ON-GNP-based therapeutic strategies to manage inflammation and disease progression in Ph-MPNs.

312

News (Medical) associated with STING

03 Apr 2025

·endpts.com

F-star management takes company private, two years after $161M cash exit to Sino's invoX

UK antibody developer F-star Therapeutics has become a private, independent biotech. The surprise move — announced via F-star’s LinkedIn page on Thursday — comes two years after a drawn-out $161 million M&A exit to invoX, a European unit of China-based Sino Biopharmaceutical. That deal went through reviews by the US’ Committee on Foreign Investment in the United States, or CFIUS. The review caused months of delays before invoX completed the acquisition in March 2023. The LinkedIn post offered few details, other than to say that the company is now owned by F-star’s management team. “We are pleased to announce that F-star Therapeutics has entered a new chapter in our history and become a private, independent company, fully owned and operated by the existing management team,” F-star wrote. F-star declined to comment on the terms of the deal or make an executive available for an interview. The biotech is led by Ryan Fiehler. Spokespeople for invoX and Sino Biopharmaceutical didn’t respond to an email inquiry from Endpoints News . F-star said in the post that it plans to continue discovering bispecific antibodies and working with partners. The company previously disclosed partnerships with Merck KGaA, Denali Therapeutics, J&J and Takeda . Those partnerships are still listed on the biotech’s website. As of the fall, according to an internet archive of the biotech’s website, F-star had three bispecific antibodies in the clinic, plus a second-generation STING agonist in Phase 1. InvoX restructured last year. It has an AI oncology partnership with Insilico Medicine.

AcquisitionPhase 1ADCImmunotherapy

26 Mar 2025

·www.legochembio.com

LigaChemBio and Partners Reveal 5 Programs Pre-clinical Results at AACR

LigaChemBio (141080KS, hereinafter 'LigaChemBio') announced on the 26th that it will present preclinical research results for five programs, including the STING agonist ‘LCB39’ under development as an immuno-oncology agent, and the LRRC15 ADC ‘SOT106’ and CA242 ADC ‘IKS04’ candidates derived through its ADC platform technology licensing, at the American Association for Cancer Research (AACR 2025) Annual Meeting. These research findings will be presented through oral presentations and posters by LigaChemBio and its partners during the AACR 2025, scheduled to be held in Chicago from April 25 to 30 (local time). The abstracts related to these presentations were made available on the conference website on the 25th. LCB39 is a next-generation immuno-oncology candidate, proprietarily developed by LigaChemBio. It targets the STING (Stimulator of Interferon Genes) protein to activate innate immune cells. STING agonists have gained attention as a promising mechanism to overcome the limitations of existing immuno-oncology drugs. However, despite numerous attempts by global pharmaceutical companies, most have failed to develop due to issues with efficacy and side effects. LigaChemBio’s LCB39 is distinctive in that it uses proprietary technology to reduce cell permeability compared to competing STING agonists, while enhancing penetration into tumor tissues and prolonging exposure. This unique approach is expected to maintain the potent efficacy of existing STING agonists while ensuring safety, increasing the likelihood of success when LCB39 enters clinical trials in early 2026, overcoming the failures of previous competitors. LigaChemBio will unveil additional data from SITC 2024, showcasing the synergistic effects of LCB39 when used in combination with various cancer treatments, including ADCs and immune checkpoint inhibitors. This data is anticipated to boost the product’s market potential given its compatibility. Furthermore, Preclinical results for 2 ADCs derived through the ADC platform licensing deals and Platform research result will also be presented. These results will be showcased by partners IKSUDA and SOTIO, which entered into ADC platform technology licensing agreements with LigaChemBio in 2020 and 2021, respectively. As these candidates are planned to enter global clinical trials, the value of the platform technology licensing is expected to be further highlighted. SOT106, currently under development by Sotio, is an ADC targeting LRRC15 (Leucine-rich repeat containing protein 15) with a monoclonal antibody and LigaChemBio’s ADC platform, 'ConjuALL', combined with an MMAE payload. It is a candidate derived from a 2021 technology licensing agreement between LigaChemBio and Sotio. LRRC15, the target of SOT106, is minimally expressed in normal tissues, but is known to be overexpressed in malignant tumors such as sarcoma, glioblastoma, head and neck squamous cell carcinoma, non-small cell lung cancer, and triple-negative breast cancer, which are cancers with high unmet medical needs. LRRC15 is considered one of the promising targets for ADC therapy development. According to the published abstract, SOT106 has demonstrated strong and sustained dose-dependent tumor growth inhibition effects in various disease-related mouse models. Complete responses were also observed at a clinically relevant dose of 1mg/kg. Notably, SOT106 showed higher efficacy with lower doses and fewer administrations compared to comparator drugs, further validating LigaChemBio’s linker technology. In addition, Sotio announced that it has developed a diagnostic antibody, which will help patient populations most likely to benefit from SOT106 treatment. This development is expected to increase the likelihood of success in the upcoming Phase 1/2 clinical trials. IKS04, currently under development by IKSUDA Therapeutics (IKSUDA), is an antibody-drug conjugate (ADC) that targets CA242 (a cancer-specific carbohydrate antigen). IKS04 combines IKSUDAs proprietary antibody with LigaChem Biosciences (LCB)'s ADC platform ConjuALL, and LCB’s proprietary payload, a PBD prodrug (Pyrrolobenzodiazepine prodrug). LCBs platforms were accessed by IKSUDA through a license agreement with LCB in 2020 for use in the development of ADCs to numerous targets. CA242, the target for IKS04, is known to be highly expressed in colorectal, pancreatic, and gastric cancers, while its expression in normal tissues is limited. Previous clinical studies, though unsuccessful, demonstrated the potential of CA242 as a druggable and potentially promising ADC target. However, these studies revealed the limitations of microtubule inhibitor-based payloads in gastric tumors due to their modest clinical efficacy. Therefore IKS04, which employs a potent DNA-damaging payload, such as a PBD, may provide significant improvement in clinical activity and offer an effective therapeutic option for patients with gastric cancers. LCBs prodrug approach enables tumor-ive release and activation of this potent payload for added safety. According to IKSUDAs published abstract, CA242 has inordinately high expression abundance in high-expressing colon and gastric models, resulting in an antigen barrier which precludes tumor penetration of the ADC. Leveraging an ‘ultra-low DAR approach through co-administration of naked antibody with the ADC, IKSUDA has demonstrated an enhancement in tumor penetration, enabling consistently low minimally effective doses of <0.5mg/kg across all CA242-expression models. As a reference, the benchmark compound cantuzumab ravtansine was inactive even at doses of 2mg/kg in these models, validating the design hypothesis for payload mechanism ion. Importantly, the ultra-low DAR approach does not negatively impact toxicity and IKS04 is also associated with a favorable preclinical therapeutic index (TI), which is significantly higher than all PBD-based ADC programs that have been assessed for solid tumors to date. In conclusion, IKS04 has demonstrated strong and consistent anti-tumor efficacy across a range of GI tumor models, including those of the stomach and colon, alongside a favorable TI. This ADC program adds further evidence of the potential clinical benefit of LCB’s proprietary PBD prodrug approach for use in ADCs to ed tumor indications. Based on these positive results, IKSUDA plans to initiate clinical trials of IKS04 using the ultra-low DAR dosage regimen in the near future. IKS04 potentially offers a new treatment option for cancers which are notoriously difficult to treat. Iksuda also presented research results that demonstrate the superiority of the linker technology introduced by LigaChemBio. According to the published abstract, Iksuda compared an FRα (Folate-Receptor Alpha) ADC using Iksuda's proprietary 'Permalink' conjugation method with LigaChemBio’s linker and MMAE payload, maintaining the antibody, conjugation method, and payload, while applying the valine-citrulline (vc) linker, which is commonly used by most global ADC companies after the expiration of its patent. Preclinical experiments showed that the ADC using LigaChemBio’s linker exhibited superior tolerability and stability in the bloodstream compared to the ADC using the vc linker. This research result is significant as it reaffirms the superiority of LigaChemBio’s proprietary linker technology over existing linker technologies

License out/inAACRADCImmunotherapy

19 Mar 2025

·www.prnewswire.com

Jacobio Pharma Announces 2024 Annual Results

BEIJING, SHANGHAI and BOSTON, March 19, 2025 /PRNewswire/ -- Jacobio Pharma (1167.HK) released its 2024 annual results, with revenue of RMB160 million, R&D expense of RMB330 million. Major operating and financing activities generated RMB320 million cash inflows. By the end of 2024, cash and bank balances and bank credit balances amounted to RMB1.45 billion. Jacobio also announced recent business progress and expected milestones. "2024 is a transforatmive year for Jacobio. We have submitted a New Drug Application (NDA) for the KRAS G12C inhibitor glecirasib and have licensed out the China rights of glecirasib and the SHP2 inhibitor sitneprotafib to our partner. This marks Jacobio's successful transformation from the early R&D stage to an innovation-driven value realization stage," said Dr.Yinxiang Wang, the Chairman and CEO of Jacobio Pharma. "Looking ahead to 2025, glecirasib is expected to receive the official approval for marking, which will continuously generate cash flow to invest in Jacobio' subsequent pipeline." Development of core clinical stage products Glecirasib (JAB-21822, KRAS G12C inhibitor) and sitneprotafib (JAB-3312, SHP2 inhibitor) The commercialization and further clinical development in China of glecirasib and sitneprotafib were licensed to Allist on August 30, 2024. Non-small cell lung cancer (NSCLC) The NDA application of glecirasib monotherapy in second-line and above NSCLC was submitted to the CDE (China Drug Evaluation Center) in May 2024 and the priority review designation was granted in the same month. Glecirasib is expected to be approved in the first half of 2025. The Phase III pivotal trial of glecirasib combined with sitneprotafib in front-line NSCLC enrolled the first patient in China on August 7, 2024. Multi-tumor basket The multi-tumor basket registration phase II trial of glecirasib for the treatment of pancreatic cancer, biliary tract cancer, gastric cancer, small bowel cancer, appendiceal cancer and other indications has been initiated in China. Glecirasib has received orphan drug designation (ODD) from FDA and EMA for pancreatic cancer. Colorectal cancer The Phase III trial of glecirasib mono or in combination with cetuximab in third line was approved by the CDE in May 2024 JAB-23E73 (pan-KRAS inhibitor) The IND (Investigational New Drug) applications were approved in China and the United States in September 2024 The first patient was enrolled in November 2024 The dose escalation phase is expected to be completed in the second half of 2025 JAB-30355 (p53 Y220C activator) The IND application of FIH (first-in-human) global trial of JAB-30355 was approved by the FDA in March 2024 and by the CDE in June 2024. The first patient was enrolled in July 2024 The dose escalation is expected to be completed in the second half of 2025 JAB-8263 (BET inhibitor) The dose escalation for JAB-8263 in solid tumors and hematologic malignancy were completed in the U.S. and China, respectively. The RP2D (phase II recommended doses) was obtained. Dose expansion in patients with myelofibrosis is ongoing. Solid tumor portion with specific biomarkers is being explored. . JAB-2485 (Aurora A inhibitor) A Phase I/IIa global trial of JAB-2485 is ongoing in the U.S. and China. Dose escalation phase is expected to be completed in the first half of 2025 The expansion of monotherapy and combination with chemotherapy are being planned. Development of pre-clinical pipelines JAB-BX467 (HER2-STING iADC) Clinical candidate of HER2-STING iADC has been nominated in the second half of 2024. The IND application is being planned to be submitted in 2026. JAB-BX600 (KRAS G12D ADC) The clinical candidate is expected to be nominated in the second half of 2025. As of December 31, 2024, Jacobio has filed more than 360 patent applications worldwide, including 126 authorized patents. Conference call information Jacobio Pharma will hold a conference call at 9:30 AM (Beijing time) on March 20, 2024. Participants, please register in advance through this link: About Jacobio Pharma Jacobio Pharma (1167.HK) is committed to providing breakthrough treatments for patients. With an induced allosteric drug discovery platform, the company's core projects focus on the KRAS pathway. The company envisions becoming a global leader in research and development, fostering strategic partnerships to drive innovation. Jacobio's R&D centers are located in Beijing, Shanghai (China), and Boston (USA). Clinical trials are conducted at over 180 sites in China, more than 30 sites in the USA, and over 10 sites across several European countries. For more information, please visit: SOURCE Jacobio Pharma WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

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