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Results for "

transcription elongation

" in MedChemExpress (MCE) Product Catalog:

25

Inhibitors & Agonists

2

Biochemical Assay Reagents

2

Peptides

2

Oligonucleotides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-153278
    Q901

    CDK7-IN-21

    		 CDK DNA/RNA Synthesis c-Myc Early 2 Factor (E2F) Topoisomerase Cancer
    Q901 (CDK7-IN-21) is a selective and potent CDK7 inhibitor with an IC50 of 10 nM. Q901 disrupts MYC and E2Ftranscription program, downregulating cell cycle control and DNA damage repair pathways. Q901 stabilizes TOP1-DPCs and sensitizes tumor to TOP1 inhibitors by suppressing RNAPII transition from initiation to elongation. Q901 can inhibit tumor growth and significantly enhances tumor growth inhibition combined with TOP1 inhibitors. Q901 can be used for the research of cancer, such as colon cancer and lung cancer .
    Q901
  • HY-103019
    Enitociclib
    2 Publications Verification

    (+)-BAY-1251152; (+)-VIP152; (S)-Enitociclib

    		 Drug Isomer CDK Apoptosis DNA/RNA Synthesis Inflammation/Immunology Cancer
    Enitociclib ((+)-BAY-1251152; (+)-VIP152) is a selective CDK9 inhibitor (IC50=3 nM) that inhibits transcriptional elongation by blocking Ser2/Ser5 phosphorylation of RNA polymerase II. Enitociclib specifically depletes key short-lived proteins such as c-MYC, MCL-1 and induces tumor cell apoptosis. Enitociclib also interferes with the production of enhancer RNAs (eRNA) and enhancer-promoter interactions, and downregulates oncogene expression at the epigenetic level. Enitociclib exerts synergistic effects with agents including Bortezomib (HY-10227), Lenalidomide (HY-A0003), Pomalidomide (HY-10984), Venetoclax (HY-15531) and Paclitaxel (HY-B0015), and even reverses paclitaxel resistance. Enitociclib serves as a vital research tool for various malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma and pancreatic ductal adenocarcinoma .
    Enitociclib
  • HY-123972
    SEC inhibitor KL-2
    1 Publications Verification

    KL-2

    		 DNA/RNA Synthesis Cancer
    SEC inhibitor KL-2 (KL-2), a peptidomimetic lead compound, is a potent, selective super elongation complex (SEC) inhibitor and disrupts the interaction between the SEC scaffolding protein AFF4 and P-TEFb, resulting in impaired release of Pol II from promoter-proximal pause sites and a reduced average rate of processive transcription elongation. SEC inhibitor KL-2 exhibits an dose-dependent inhibitory effect on AFF4-CCNT1 interaction with a Ki of 1.50 μM .
    SEC inhibitor KL-2
  • HY-120118
    Metarrestin

    ML246

    		 DNA/RNA Synthesis Cancer
    Metarrestin (ML246) is an orally active, first-in-class and specific perinucleolar compartment inhibitor. Metarrestin disrupts the nucleolar structure and inhibits RNA polymerase (Pol) I transcription, at least in part by interacting with the translation elongation factor eEF1A2. Metarrestin blocks metastatic development and extends survival in mouse cancer models .
    Metarrestin
  • HY-143584
    AZ5576

    		CDK Apoptosis Cancer
    AZ5576 is a potent and highly selective CDK9 inhibitor (IC50: <5 nM). AZ5576 inhibits the phosphorylation of RNA polymerase II at Ser2, thereby inhibiting transcriptional elongation. AZ5576 can be used for hematological Malignancy research .
    AZ5576
  • HY-162350
    TDI-11055

    		Epigenetic Reader Domain Apoptosis Cancer
    TDI-11055 is a selective and orally active eleven-nineteen leukemia (ENL) inhibitor, which displaces ENL from chromatin by blocking its YEATS domain interaction with acylated histones. TDI-11055 inhibits ENL and AF9 YEATS domains with IC50 values of 50 nM and 70 nM, respectively, and no activity against GAS41 or YEATS2. TDI-11055 decreases chromatin occupancy of ENL-associated complexes, impairs transcription elongation, suppresses key oncogenic gene expression programs, and induces differentiation. TDI-11055 can be used for the research of acute myeloid leukemia .
    TDI-11055
  • HY-141567A
    Pseudouridine 5'-triphosphate trisodium solution (100 mM)
    1 Publications Verification

    Pseudo-UTP trisodium solution (100 mM)

    		 DNA/RNA Synthesis Infection
    Pseudouridine 5'-triphosphate (Pseudo-UTP) trisodium solution (100 mM) is a modified ribonucleoside triphosphate and uracil base-modified UTP derivative. Pseudouridine 5'-triphosphate trisodium solution (100 mM) enhances translational properties and stability of mRNA, reduces innate immune responses in mammalian cells, and inhibits signal-dependent transcription termination of vaccinia virus early gene transcription while supporting transcription elongation. Pseudouridine 5'-triphosphate trisodium solution (100 mM) can be used for the research of vaccinia virus infection .
    Pseudouridine 5'-triphosphate trisodium solution (100 mM)
  • HY-126428
    ZL0580
    1 Publications Verification

    		 HIV Epigenetic Reader Domain Infection Inflammation/Immunology
    ZL0580, a structurally close analog of ZL0590, induces epigenetic suppression of HIV via selectively binding to BD1 domain of BRD4. ZL0580 induces HIV suppression by inhibiting Tat transactivation and transcription elongation as well as by inducing repressive chromatin structure at the HIV promoter .
    ZL0580
  • HY-141567
    Pseudouridine 5'-triphosphate

    Pseudo-UTP

    		 DNA/RNA Synthesis Infection
    Pseudouridine 5'-triphosphate (Pseudo-UTP) is a modified ribonucleoside triphosphate and uracil base-modified UTP derivative. Pseudouridine 5'-triphosphate enhances translational properties and stability of mRNA, reduces innate immune responses in mammalian cells, and inhibits signal-dependent transcription termination of vaccinia virus early gene transcription while supporting transcription elongation. Pseudouridine 5'-triphosphate can be used for the research of vaccinia virus infection .
    Pseudouridine 5'-triphosphate
  • HY-168556
    YJ9069

    		CDK PROTACs DNA/RNA Synthesis Cancer
    YJ9069 is a selective CDK12/CDK13 PROTAC degrader with an IC50 of 22.22 nM for in VCaP cells. CDK12/13 degradation rapidly triggers gene-length-dependent transcriptional elongation defects, leading to DNA damage and cell-cycle arrest. YJ9069 effectively inhibits proliferation in subsets of prostate cancer cells and significantly suppresses prostate tumor growth. (Pink: CDK12/CDK13 degradation agent (HY-168658); Black: Linker (HY-W015967); Blue: ligand for E3 ligase (HY-103596)) .
    YJ9069
  • HY-169093
    MS41

    		PROTACs Epigenetic Reader Domain Apoptosis Cancer
    MS41 is a selective eleven-nineteen leukemia (ENL) PROTAC degrader, with DC50s of 3.50 nM (MV4;11), 2.84 nM (SEMK2), 3.03 nM (Jurkat), and 26.58 nM (KASUMI1), respectively. MS41 effectively inhibits the growth of ENL-dependent leukemia cells, induces G1 cell cycle arrest and increases apoptosis. MS41 reduces the chromatin occupancy of ENL-associated transcription elongation machinery, and suppresses oncogenic gene expression and leukemia progression. Red: ENL ligand (HY-169094). Black: linker (HY-W105744). Blue: VHL ligand (HY-112078) .
    MS41
  • HY-161771
    JNJ-7184

    		RSV Infection
    JNJ-7184 is a non-nucleoside inhibitor of the RSV-Large (L) polymerase, with the pEC50 and pCC50 of 7.86 and 4.29 in Hela cells, respectively. JNJ-7184 prevents RSV replication and transcription by inhibiting initiation or early elongation .
    JNJ-7184
  • HY-153278A
    Q901 TFA

    CDK7-IN-21 TFA

    		 CDK DNA/RNA Synthesis c-Myc Early 2 Factor (E2F) Topoisomerase Cancer
    Q901 (CDK7-IN-21) TFA is a selective and potent CDK7 inhibitor with an IC50 of 10 nM. Q901 TFA disrupts MYC and E2Ftranscription program, downregulating cell cycle control and DNA damage repair pathways. Q901 TFA stabilizes TOP1-DPCs and sensitizes tumor to TOP1 inhibitors by suppressing RNAPII transition from initiation to elongation. Q901 TFA can inhibit tumor growth and significantly enhances tumor growth inhibition combined with TOP1 inhibitors. Q901 TFA can be used for the research of cancer, such as colon cancer and lung cancer .
    Q901 TFA
  • HY-E70659
    CDK12/CycK Recombinant Human Active Protein Kinase

    		CDK Cancer
    CDK12/CycK Recombinant Human Active Protein Kinase is a cyclin-dependent kinase that phosphorylates the C-terminal domain (CTD) of RNA polymerase II (Pol II), thereby regulating different phases of the transcription cycle from transcription initiation to elongation and termination .
    CDK12/CycK Recombinant Human Active Protein Kinase
  • HY-178499
    CDK9-IN-44

    		CDK c-Myc Bcl-2 Family Neurological Disease Cancer
    CDK9-IN-44 (Compound 7) is a selective CDK9 inhibitor (IC50=7.6 μM). CDK9-IN-44 inhibits CDK9/cyclin T1 kinase activity, blocking transcriptional elongation, reducing the expression of pro-cancer proteins (such as MCL1, c-MYC), and inducing tumor cell apoptosis. CDK9-IN-44 is promising for research of glioblastoma (GBM) and central nervous system (CNS) disorders .
    CDK9-IN-44
  • HY-171786
    CDK12-IN-8

    		CDK Cancer
    CDK12-IN-8 (Compound Cpd143) is an orally active and highly selective inhibitor of cyclin-dependent kinase 12 (CDK12). CDK12-IN-8 inhibits CDK12-mediated phosphorylation of the C-terminal domain (CTD) serine 2 of RNA polymerase II, interfering with gene transcription elongation and DNA damage repair pathways. CDK12-IN-8 is promising for research of cancers with high CDK12 expression such as small cell lung cancer and triple-negative breast cancer .
    CDK12-IN-8
  • HY-P3103
    PINT-87aa

    		DNA/RNA Synthesis Cancer
    PINT-87aa, an 87-amino acid (aa) peptide, is encoded by the circular form of the long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT). PINT-87aa directly interacts with polymerase associated factor complex (PAF1c) and inhibits the transcriptional elongation of multiple oncogenes. PINT-87aa suppresses glioblastoma cell proliferation in vitro and in vivo .
    PINT-87aa
  • HY-P3103A
    PINT-87aa TFA

    		DNA/RNA Synthesis Cancer
    PINT-87aa TFA, an 87-amino acid (aa) peptide, is encoded by the circular form of the long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT). PINT-87aa TFA directly interacts with polymerase associated factor complex (PAF1c) and inhibits the transcriptional elongation of multiple oncogenes. PINT-87aa TFA suppresses glioblastoma cell proliferation in vitro and in vivo .
    PINT-87aa TFA
  • HY-171632
    2'-(2-Nitrobenzyl)-ATP

    		DNA/RNA Synthesis Biochemical Assay Reagents Others
    2'-(2-Nitrobenzyl)-ATP is an rATP analog. 2'-(2-Nitrobenzyl)-ATP acts as a transcription terminator, inhibiting further RNA chain elongation by T7 RNA polymerase .
    2'-(2-Nitrobenzyl)-ATP
  • HY-171632A
    2'-(2-Nitrobenzyl)-ATP trisodium

    		DNA/RNA Synthesis Biochemical Assay Reagents Others
    2'-(2-Nitrobenzyl)-ATP trisodium is a rATP analog. 2'-(2-Nitrobenzyl)-ATP trisodium acts as a transcription terminator, inhibiting further RNA chain elongation by T7 RNA polymerase .
    2'-(2-Nitrobenzyl)-ATP trisodium
  • HY-173147
    CDK2-IN-42

    		CDK Cancer
    CDK2-IN-42 (Compound H63) is a CDK12 inhibitor with an IC50 value of 10 nM. CDK2-IN-42 has anti-ESCC (Esophageal Squamous Cell Carcinoma) cell activity. It can block transcriptional elongation, downregulate the core genes in the G1 phase to induce cell cycle arrest, and alter the CDK12-ATM/ATR-CHEK1/CHEK2 signaling axis, resulting in DNA damage. CDK2-IN-42 can effectively inhibit tumor growth in a xenograft mouse model of human ESCC KYSE150. CDK2-IN-42 holds great promise for research in the field of cancer .
    CDK2-IN-42
  • HY-181831
    XQ2

    		Drug Derivative HIV Epigenetic Reader Domain Infection
    XQ2 is a resveratrol (HY-16561) derivative and latency-reversing agent. XQ2 releases positive transcription elongation factor b (P-TEFb) from BRD4, thereby promoting Tat-dependent viral transcription. XQ2 reactivates latent HIV-1 via activating P-TEFb .
    XQ2
  • HY-181231
    PROTAC CDK9 degrader-12

    		PROTACs CDK HIV DNA/RNA Synthesis Infection
    PROTAC CDK9 degrader-12 is a selective CDK9 PROTAC degrader with a DC50 of 23 nM. PROTAC CDK9 degrader-12 induces proteasome-dependent degradation of CDK9, blocks CDK9-mediated HIV-1 transcriptional elongation, and reduces HIV-1 RNA synthesis. PROTAC CDK9 degrader-12 is applicable to research related to HIV-1 infection .
    PROTAC CDK9 degrader-12
  • HY-181275
    CDK9 ligand 4

    		Ligands for Target Protein for PROTAC CDK HIV Infection
    CDK9 ligand 4 is a CDK9 ligand. As a ligand for target protein for PROTAC (Ligands for Target Protein for PROTAC), CDK9 ligand 4 serves for the development and design of PROTAC CDK9 degraders, such as PROTAC CDK9 degrader-12 (HY-181231). CDK9 ligand 4 is applicable to the research of HIV-1 infection .
    CDK9 ligand 4
  • HY-103019R
    Enitociclib (Standard)

    (+)-BAY-1251152 (Standard); (+)-VIP152 (Standard); (S)-Enitociclib (Standard)

    		 Reference Standards Drug Isomer Apoptosis DNA/RNA Synthesis CDK Cancer
    Enitociclib (Standard) is the analytical standard of Enitociclib (HY-103019). This product is intended for research and analytical applications. Enitociclib ((+)-BAY-1251152; (+)-VIP152) is a selective CDK9 inhibitor (IC50=3 nM) that inhibits transcriptional elongation by blocking Ser2/Ser5 phosphorylation of RNA polymerase II. Enitociclib specifically depletes key short-lived proteins such as c-MYC, MCL-1 and induces tumor cell apoptosis. Enitociclib also interferes with the production of enhancer RNAs (eRNA) and enhancer-promoter interactions, and downregulates oncogene expression at the epigenetic level. Enitociclib exerts synergistic effects with agents including Bortezomib (HY-10227), Lenalidomide (HY-A0003), Pomalidomide (HY-10984), Venetoclax (HY-15531) and Paclitaxel (HY-B0015), and even reverses paclitaxel resistance. Enitociclib serves as a vital research tool for various malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma and pancreatic ductal adenocarcinoma .
    Enitociclib (Standard)

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