NCT06626633

2321GCCC: CRD3874-SI in Patients With Relapsed/Refractory AML

Suspended Phase 1 Last updated 12 March 2026

What this trial tests

Phase 1 trial testing CRD3874 in Acute Myeloid Leukemia in 6 participants. Suspended.

Timeline

26 August 2024

Primary endpoint
25 August 2025

31 January 2028

Quick facts

Lead sponsor	University of Maryland, Baltimore
Phase	Phase 1
Status	Suspended
Study type	INTERVENTIONAL
Allocation	na
Design	single group
Masking	none
Primary purpose	treatment
Enrollment	6
Start date	26 August 2024
Primary completion	25 August 2025
Estimated completion	31 January 2028
Sites	1 location across United States

Drugs / interventions tested

• CRD3874 — full drug profile →

Conditions studied

• Acute Myeloid Leukemia — all drugs for Acute Myeloid Leukemia →

Sponsor

University of Maryland, Baltimore

Who can join

18 and older, any sex, with Acute Myeloid Leukemia. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

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.

Publications & conference data

8 peer-reviewed publications reference this trial (live from Europe PMC):

1. Demystifying the cGAS-STING pathway: precision regulation in the tumor immune microenvironment.
   Wang Q, Yu Y, Zhuang J, Liu R, et al · · 2025 · cited 27× · PMID 40506729 · DOI 10.1186/s12943-025-02380-0
2. Nanomedicines harnessing cGAS-STING pathway: sparking immune revitalization to transform 'cold' tumors into 'hot' tumors.
   Ying X, Chen Q, Yang Y, Wu Z, et al · · 2024 · cited 26× · PMID 39710707 · DOI 10.1186/s12943-024-02186-6
3. Enhancing radiotherapy-induced anti-tumor immunity via nanoparticle-mediated STING agonist synergy.
   Zeng Q, Liu M, Wang Z, Zhou R, et al · · 2025 · cited 12× · PMID 40500702 · DOI 10.1186/s12943-025-02366-y
4. Phase 1 first-in-human dose-escalation study of IMSA101, a novel cyclic di-nucleotide STING agonist, for patients with advanced solid tumor malignancies.
   Jacoby J, Mahalingam D, Alistar A, Garmey E, et al · · 2025 · cited 11× · PMID 40533265 · DOI 10.1136/jitc-2025-011572
5. Progress Update on STING Agonists as Vaccine Adjuvants.
   Shen Y, Huang W, Nie J, Zhang L. · · 2025 · cited 9× · PMID 40333245 · DOI 10.3390/vaccines13040371
6. Emerging cGAS-STING Agonist-Based Nanotherapeutics: Mechanistic Insights and Applications in Cancer Combination Therapy.
   Wang Z, Wang Y, He Z, Liu C. · · 2025 · cited 5× · PMID 40842018 · DOI 10.1002/advs.202509890
7. Conjugated STING agonists.
   Qu S, Dai H. · · 2025 · cited 4× · PMID 40291379 · DOI 10.1016/j.omtn.2025.102530
8. Identification of a Novel Small Molecule STING Agonist Reshaping the Immunomicroenvironment of Pancreatic Ductal Adenocarcinoma.
   Liu P, Shi M, Liu Y, Liu Y, et al · · 2025 · cited 3× · PMID 40520004 · DOI 10.7150/ijbs.107837