Drug Database
TR

trans-retinoic acid (tretinoin, Heron / Renova, Micro)

✓ Approved

Johnson & Johnson Services, Inc. · therapeutic agent

What is trans-retinoic acid?

trans-retinoic acid is a therapeutic agent developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via topical.

Drug Profile

Brand Namestretinoin, Heron, Renova, Micro
CompanyJohnson & Johnson Services, Inc.
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Therapeutic Indications

trans-retinoic acid is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersAcne✓ Approved

Related Research Articles

PubMedMedicine2026-11-11

Pulmonary embolism as the initial manifestation of acute promyelocytic leukemia: A case report and review of the literature.

Dong Jiayao J, Zhai Xiao X

Acute promyelocytic leukemia (APL) usually presents with bleeding-related coagulopathy. Pulmonary embolism (PE) before APL is recognized is uncommon and complicates anticoagulation. A 26-year-old obese man presented with progressive dyspnea, small-volume hemoptysis, and pleuritic chest pain. Computed tomography pulmonary angiography showed segmental PE in the right lower lobe. Leukocytosis, anemia, and severe thrombocytopenia prompted hematologic evaluation. Bone marrow morphology, t(15;17), and promyelocytic leukemia-retinoic acid receptor alpha confirmed high-risk APL. Nadroparin was started for PE. After APL was confirmed, all-trans retinoic acid, hydroxyurea, pirarubicin, and later arsenic trioxide were administered. Anticoagulation was reduced during bleeding and thrombocytopenia and later resumed with transfusion support. Suspected differentiation syndrome resolved with dexamethasone. PE improved, but a splenic infarct developed during induction. Therapeutic anticoagulation was resumed after bleeding resolved. The patient achieved sustained molecular remission, complete radiologic resolution of PE, and no recurrent thrombosis during more than 2.5 years of follow-up. PE with unexplained cytopenias or leukocytosis should prompt smear review and urgent evaluation for APL. Confirmed thrombosis requires anticoagulation individualized to thrombus severity, bleeding, platelet and fibrinogen trends, and serial reassessment.

PMID 43012828
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PubMedRSC medicinal chemistry2026-11-11

Expanding the chemical space of guanidinium-stapled peptides with aromatic residues yields NCOA mimics with high affinity for nuclear receptors.

Trousselier Pauline P, Silvestri Aurora A, Peluso-Iltis Carole C, Osz Judit J et al.

Macrocyclization via guanidinium stapling is a modular synthetic approach to stabilize α-helical peptides and create constrained arginine mimics, while introducing positively charged, hydrogen-bonding moieties. To expand the structural diversity of guanidinium-stapled peptides, we incorporated non-natural amino acids, p-azidomethyl-l-phenylalanine (F*) and O-(2-azidoethyl)-l-tyrosine (Y*), to introduce aromatic groups into the macrocycle. We demonstrate compatibility with (i, i + 4) and (i, i + 7) stapling geometries and apply this approach to mimic nuclear receptor coactivator (NCOA) peptides for binding to human nuclear hormone receptors (NHR), including retinoic acid receptor alpha (RARα) and vitamin D receptor (VDR). Our structural and biophysical analyses reveal that aromatic elements within the guanidinium staple can modulate helical stability, enhance binding affinity, and contribute direct interactions with the protein surface.

PMID 43011727
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PubMedJournal of nanobiotechnology2026-11-11

A quantitative and visual detection probe based on isothermal nucleic acid amplification coupled with CRISPR/Cas12a system (INACS) for miR155 detection.

Ma Yunsu Y, Li Jing J, Jin Xiaojuan X, Liu Sunan S et al.

MicroRNAs (miRNAs) have emerged as ideal biomarkers for early clinical diagnosis. Achieving the accurate detection of miRNAs plays a critical role for assuring its implementation in their clinical applications. In this study, we developed a dual-signal amplified ultrasensitive fluorescent sensing platform for miR155 detection by coupling isothermal nucleic acid amplification with the CRISPR/Cas12a system (INACS). Using a hairpin nucleic acid probe (HP) as the substrate, the system specifically recognizes the target miR155, triggering the opening of the hairpin loop structure. Subsequently, under the catalysis of Bst DNA polymerase, target gene amplification produces dsDNA with a specific sequence. This dsDNA activates the trans-cleavage activity of Cas12a, which cleaves reporter strands labeled with quencher and fluorescent groups, restoring the fluorescence signal. The fluorescence intensity is proportional to miR155 concentration, exhibiting a strong linear relationship between fluorescence intensity ratio and the logarithm of miR155 concentration over the range of 0.5-50 pM (r = 0.9961). By integrating nucleic acid amplification with CRISPR/Cas12a amplification, INACS achieves high sensitivity, excellent selectivity, and a detection limit as low as 34.46 fM. INACS was successfully applied to human serum samples, revealing elevated miR155 levels in breast cancer patients compared to non-cancer controls. Moreover, INACS was adapted for semi-quantitative detection using lateral flow assay (LFA) test strips. Results were assessed by naked-eye color comparison, facilitating rapid onsite auxiliary diagnosis of breast cancer. The LFA outcomes were consistent with serum fluorescence measurements, enabling efficient and user-friendly visual detection. This work thus provides a promising tool for early clinical diagnosis.

PMID 43009987
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PubMedNucleic acids research2026-11-11

A RARγ-SMARCA5 chromatin-remodeling axis stabilizes AR luminal programs and opposes lineage plasticity in prostate cancer.

Wani Sajad A SA, Hussain Shahid S, Mir Khalid B KB, Gray Jaimie S JS et al.

In prostate cancer (PCa), epigenomic mechanisms drive resistance to androgen receptor (AR) signaling inhibitors, such as enzalutamide (enza). We tested whether retinoic acid receptor gamma (RARγ) shapes the epigenome to direct AR transcription, promote luminal identity, and limit enza resistance. RARγ restoration in enza-resistant 22Rv1 cells induced a large RARγ complex containing its coactivator TACC1 and the chromatin remodeler ISWI ATPase SMARCA5. RARγ restoration expanded and redistributed the AR cistrome toward active promoters, enhancers, and unique super-enhancers and increased the overlap with H3K27ac. RARγ restoration also increased SMARCA5 promoter-proximal binding that overlapped with G2/M-enriched AR cistrome, linking AR redistribution to cell cycle-associated chromatin engagement, including at luminal genes. In 22Rv1 and LNCaP C4-2 (also enza-resistant), RARγ restoration directed the AR transcriptome toward luminal differentiation. A miR-96 antagomir (targeting RARγ) mirrored the impact of RARγ restoration. RARγ antagonized the actions of the master lineage regulator ONECUT2 at the cistrome and transcriptome level and these antagonized genes were significantly associated with alternative lineages in murine PCa models of lineage plasticity and enza responsiveness and lineage plasticity in human PCa cohorts. These findings identify RARγ as a regulator of a chromatin remodeling mechanism that sustains luminal AR programs and opposes therapeutic resistance.

PMID 43010877
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PubMedAnatolian journal of cardiology2026-11-11

Circulating Quiescin Sulfhydryl Oxidase and Risk of Cardiovascular Disease: A Mendelian Randomization and Post-GWAS Analysis.

Che Xinyu X, Chen Ao A, Xia Yan Y, Yang Zheng Z et al.

To systematically evaluate the causal associations between circulating quiescin sulfhydryl oxidase (QSOX) family enzymes and cardiovascular diseases (CVDs) using Mendelian randomization (MR) and post-Genome-Wide Association Study (post-GWAS) analyses. The authors integrated protein quantitative trait locus (pQTL) data for plasma QSOX from the INTERVAL and deCODE studies with CVD GWAS summary statistics from large‑scale biobank datasets and disease‑specific consortia. Discovery MR analyses were followed by meta-analysis and independent replication. Post-GWAS annotation using the FUMA platform was performed to delineate the pQTL architecture of circulating QSOX2 and to prioritize likely causal variants. Summary-data-based Mendelian randomization (SMR) was applied to confirm direct effects of QSOX2 on CVDs and to characterize its regulatory networks at individual cis and trans pQTLs. Initial pan-MR analyses suggested risk-increasing associations of circulating QSOX2 with several CVDs, but showed substantial SNP-level heterogeneity. Regional and functional annotation identified pleiotropic signals originating from distal and trans regions, and prioritized the missense variant rs12380852 as the leading causal candidate, predicted to impair QSOX2 structural stability and enzymatic activity. Notably, cis-MR and SMR analyses restricted to the QSOX2 locus revealed consistent protective effects against atrial fibrillation (AF) and heart failure (HF). Summary‑data-based Mendelian randomization on trans pQTL rs3184504 (a SH2B3 missense variant) linked SH2B3‑mediated inflammatory pathways to QSOX2 trans regulation. The authors' findings suggest a protective role of circulating QSOX2 in AF and HF. The prioritized causal variants and identified trans-regulatory pathways may serve as targets for future functional validation and druggable design. #Xinyu Che, Ao Chen, and Yan Xia contributed equally to this work.

PMID 43012472
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PubMedAnalytical chemistry2026-11-11

Programming CRISPR Compartmentalization on DNA Origami for Multiplexed Biosensing.

Capelli Luca L, Hao Yaya Y, Shi Qien Q, Li Qian Q et al.

CRISPR-Cas12a has emerged as a transformative tool for nucleic acid detection and molecular diagnostics. However, achieving one-pot, orthogonal, multiplexed sensing remains challenging due to the nonspecific trans-cleavage activity of Cas12a. Here, we present a modular DNA origami-based platform that spatially confines and independently controls Cas12a activity, enabling simultaneous detection of multiple DNA targets within a single reaction. This spatial programming approach enables orthogonal one-pot detection of three DNA targets (EGFR L858R/Del19 mutations and HPV16) with minimal cross-talk, demonstrating 60% cleavage efficiency within 120 min at 100 nM. Through integrated molecular dynamics simulations and experimental validation, we identify an optimal ∼6 nm spatial window that maximizes cleavage efficiency, while the platform maintains robust performance in complex biological environments with a 10 nM detection limit in 20% serum. This compartmentalization strategy establishes a framework for spatially programming multi-enzyme systems on DNA nanostructures for synthetic biological circuits.

PMID 43010433
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