2. Academic Validation
  3. XQ2, a Novel Derivative of Resveratrol, Reactivates Latent HIV‑1 via the Activation of Positive Transcription Elongation Factor B

XQ2, a Novel Derivative of Resveratrol, Reactivates Latent HIV‑1 via the Activation of Positive Transcription Elongation Factor B

  • ACS Omega. 2026 Feb 11;11(7):11739-11752. doi: 10.1021/acsomega.5c10420.
Fangyuan Lai 1 2,  Chenliang Zhou 1 3,  Hong He 1,  Ziyao Wu 1,  Huba Khamis Rashid 1,  Pei Chen 1 4,  Wenli Liu 1,  Taizhen Liang 1,  Chao Li 5,  Baomin Xi 1,  Yibin Li 1,  Lin Li 1
Affiliations

Affiliations

  • 1 Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Drug Metabolism, Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, P. R. China.
  • 2 Department of Pharmacy, Shenzhen Children's Hospital, Shenzhen 518000, P. R. China.
  • 3 College of Pharmacy, Nanchang Medical College, Nanchang 330052, P. R. China.
  • 4 Zhaoqing Medical College Zhaoqing 526020 P. R. China.
  • 5 Hubei Bio-Pharmaceutical Industrial Technological Institute Inc, Wuhan, Hubei 430000, P. R. China.
PMID: 41768657 DOI: 10.1021/acsomega.5c10420
Abstract

The persistence of latent reservoirs remains the primary barrier to HIV-1 eradication. Although diverse latency-reversing agents (LRAs) have been designed to induce latent HIV-1 expression, their clinical utility is frequently limited by significant toxicity or insufficient potency. Our previous research confirmed that resveratrol reverses latent HIV-1 expression in vitro by regulating multiple signaling pathways. Based on the chemical structure of resveratrol, we designed and synthesized a small-molecule compound, XQ2 (5,7-dimethoxy-2-[5-(Ethoxymethyl)-2-furanyl]-4-(3H)-quinazolinone). Current data indicate that XQ2 efficiently promotes viral reactivation in latently infected cell models while maintaining low cytotoxicity and avoiding broad T-cell stimulation. Significantly, XQ2 demonstrates synergistic potential when administered alongside several typical LRAs. The mechanism driving XQ2-mediated reactivation appears to involve the release of positive transcription elongation factor b (P-TEFb) from bromodomain 4 (BRD4), facilitating Tat-dependent viral transcription. These results suggest that XQ2 is a promising, low-toxicity LRA candidate for advancing the "shock and kill" eradication strategy.

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