HIV-1
HIV-1 is a retrovirus whose replication relies on reverse transcription of viral RNA into DNA, integrating into host genomes to produce progeny virions[1]. Viral entry is mediated by interactions between the envelope glycoprotein gp120 and the host CD4 receptor, along with chemokine co-receptors CXCR4 or CCR5, triggering membrane fusion and infection of target cells[2][3]. Post-entry, reverse transcription and integration involve complex protein-nucleic acid interactions, with viral integrase and nucleocapsid proteins directing efficient DNA synthesis[4]. The viral replication cycle engages host signaling pathways, including calcium-dependent activation cascades, nitric oxide signaling, and protein kinase C isoforms, which modulate viral transcription and assembly[5][6]. HIV-1 accessory proteins, such as Nef and Vif, interact with host factors to enhance replication and evade immune detection, establishing persistent infection[7]. Compared with related retroviruses, HIV-1 exhibits unique isoform-specific interactions of its envelope and regulatory proteins with host pathways, enabling differential cellular tropism and pathogenicity[1]. Small molecule inhibitors and peptide agonists targeting gp120-CD4 binding, integrase activity, or host signaling components have been employed to dissect viral replication mechanisms in vitro and in vivo, providing tools for experimental modulation of viral processes[8][9]. Mechanistically, selective modulation of these pathways has been used to evaluate antiviral efficacy and to define host determinants of infection, highlighting the functional distinctions among viral isoforms and their cellular interactions[10][11].
References:
- [1]. Downey GP, et al. Chemotactic peptide-induced activation of MEK-2, the predominant isoform in human neutrophils. Inhibition by wortmannin. J Biol Chem. 1996 Aug 30;271(35):21005-1011. [Content Brief]
- [2]. Boyé K, et al. Ligand activation induces different conformational changes in CXCR3 receptor isoforms as evidenced by plasmon waveguide resonance (PWR). Sci Rep. 2017 Sep 6;7(1):10703. [Content Brief]
- [3]. Karaś K, et al. The Dichotomous Nature of AZ5104 (an EGFR Inhibitor) Towards RORγ and RORγT. Int J Mol Sci. 2019 Nov 17;20(22):5780. [Content Brief]
- [4]. Maroney SA, et al. New insights into the biology of tissue factor pathway inhibitor. J Thromb Haemost. 2015 Jun;13 Suppl 1(0 1):S200-7. [Content Brief]
- [5]. Mourelle M, et al. The arginine/nitric oxide pathway modulates sphincter of Oddi motor activity in guinea pigs and rabbits. Gastroenterology. 1993 Nov;105(5):1299-305. [Content Brief]
- [6]. Liang C, et al. Rosiglitazone via upregulation of Akt/eNOS pathways attenuates dysfunction of endothelial progenitor cells, induced by advanced glycation end products. Br J Pharmacol. 2009 Dec;158(8):1865-73. [Content Brief]
- [7]. Kampa M, et al. Opioids are non-competitive inhibitors of nitric oxide synthase in T47D human breast cancer cells. Cell Death Differ. 2001 Sep;8(9):943-52. [Content Brief]
- [8]. Jing Q, et al. In search of potent and selective inhibitors of neuronal nitric oxide synthase with more simple structures. Bioorg Med Chem. 2013 Sep 1;21(17):5323-31. [Content Brief]
- [9]. Courilleau D, et al. The (R)-enantiomer of CE3F4 is a preferential inhibitor of human exchange protein directly activated by cyclic AMP isoform 1 (Epac1). Biochem Biophys Res Commun. 2013 Oct 25;440(3):443-8. [Content Brief]
- [10]. Shih CD. Activation of estrogen receptor beta-dependent nitric oxide signaling mediates the hypotensive effects of estrogen in the rostral ventrolateral medulla of anesthetized rats. J Biomed Sci. 2009 Jul 7;16(1):60. doi: 10.1186/1423-0127-16-60. PMID: 19583861; PMCID: PMC2717931. et al. Activation of estrogen receptor beta-dependent nitric oxide signaling mediates the hypotensive effects of estrogen in the rostral ventrolateral medulla of anesthetized rats. J Biomed Sci. 2009 Jul 7;16(1):60. [Content Brief]
- [11]. Larivière S, et al. Gonadotropin-releasing hormone inhibits pituitary adenylyl cyclase-activating polypeptide coupling to 3',5'-cyclic adenosine-5'-monophosphate pathway in LbetaT2 gonadotrope cells through novel protein kinase C isoforms and phosphorylation of pituitary adenylyl cyclase-activating polypeptide type I receptor. Endocrinology. 2008 Dec;149(12):6389-98. [Content Brief]
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HIV-1 Related Products (414)
Related Products (414)
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Pancracine
0 ImagesCat. No.: HY-N20721CAS No.: 21416-14-8Pancracine is an alkaloid. Pancracine upregulates p27, phosphorylated p38 MAPK and phosphorylated p53, while downregulating phosphorylated Akt and phosphorylated Rb. Pancracine induces G1 cell cycle arrest and Apoptosis in cells. Pancracine inhibits the replication of pseudotyped HIV-1 and Dengue virus. Pancracine can be used in research related to lung adenocarcinoma, acute lymphoblastic leukemia, cutaneous epidermoid carcinoma, human immunodeficiency virus infection and dengue virus infection.
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DIBA-1
0 ImagesCat. No.: HY-123048CAS No.: 171744-39-1Synonyms: PD022551; NSC 654077DIBA-1 (PD022551; NSC 654077) is an inhibitor of HIV-1 nucleocapsid protein (NCp7). DIBA-1 displaces zinc from the zinc finger motifs of NCp7, p7NC and Pr55gag via thiol-disulfide exchange, covalently modifies cysteine residues, forms intermolecular disulfide cross-links, and disrupts zinc coordination. DIBA-1 inhibits zinc-dependent binding of NCp7 to HIV Ψ RNA, blocks the early replication process of HIV-1, suppresses the proteolytic processing of Gag precursors, and impairs the maturation and release of viral particles. DIBA-1 can be used in studies related to human immunodeficiency virus type 1 infection.
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U 80493
0 ImagesCat. No.: HY-183886CAS No.: 136816-67-6U 80493 is a HIV-1 reverse transcriptase inhibitor with IC50 of 20 μM. U 80493 can be used for the research of acquired immunodeficiency syndrome.
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KNI-174
0 ImagesCat. No.: HY-187630CAS No.: 141804-42-4
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TLR8 agonist 10
0 ImagesCat. No.: HY-181841CAS No.: 2796210-93-8TLR8 agonist 10 is a selective TLR8 agonist with an EC50 of 0.019 μM in humans. TLR8 agonist 10 activates TLR8-mediated signaling pathways. As a latency-reversing agent, TLR8 agonist 10 reactivates latent HIV-1 reservoirs. TLR8 agonist 10 activates innate cytotoxic natural killer cells to target HIV-infected CD4+ T cells. TLR8 agonist 10 is applicable to research related to HIV-1 infection.
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E913
0 ImagesCat. No.: HY-118962CAS No.: 342394-93-8E913 is a CCR5 antagonist that competes with the binding of antibodies to CCR5 which recognize the C-terminal half of the second extracellular loop (ECL2B) of CCR5. E913 can specifically block the binding of macrophage inflammatory protein-1alpha (MIP-1alpha) to CCR5 (IC50 = 0.002 μM) and MIP-1alpha-elicited cellular Ca2+ mobilization (IC50 = 0.02 μM). E913 inhibits the replication of laboratory and primary R5 HIV-1 strains as well as various multidrug-resistant monocyte/macrophage tropic (R5) HIV-1 (IC50 = 0.03-0.06 μM). E913 can be used for the research of infection, such as HIV-1 infection.
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JTK-101
0 ImagesCat. No.: HY-119120CAS No.: 503048-34-8
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GRL-142
0 ImagesCat. No.: HY-181888GRL-142 is a potent HIV-1 protease inhibitor capable of crossing the blood-brain barrier. GRL-142 exhibits extremely high inhibitory activity against both wild-type and multidrug-resistant strains (IC50=0.0094 nM). GRL-142 acts synergistically with the P2/P2' segments via a unique scaffold binding mechanism, utilizes fluorine-mediated stable interactions to maintain its bioactive conformation, adapts to p51 HIV-1 protease mutants, and maintains the flap-closed state by directly acting on the flap tip residues. GRL-142 disrupts the flap-water hydrogen bond network of wild-type protease, thereby effectively blocking viral replication. GRL-142 can be used to study HIV-1 infection and the associated neurocognitive disorder (HAND).
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HIV-1-IN-85
0 ImagesCat. No.: HY-175491HIV-1-IN-85 is an orally active HIV-1 inhibitor (IC50 = 72 nM). HIV-1-IN-85 exhibits strong inhibitory activity against wild-type (WT) HIV-1 and NNRTI-resistant single mutant strains (L100I, K103N, Y181C, Y188L, E138K) and moderate efficacy against double mutant strains (F227L+V106A, RES056). HIV-1-IN-85 shows good in vivo safety in ICR mice. HIV-1-IN-85 can be used for the study of HIV-1 infection.
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RDEA-427
0 ImagesCat. No.: HY-111147CAS No.: 914496-19-8RDEA-427 is a pyrrolopyrimidine derivative and also a HIV-1 non-nucleoside reverse transcriptase inhibitor (NNRTI). RDEA-427 acts on wild-type and NNRTI-resistant mutant HIV-1. RDEA-427 can be used in research related to HIV infection.
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Schirubridilactone D
0 ImagesCat. No.: HY-N19901CAS No.: 1210051-95-8Schirubridilactone D is a HIV-1 inhibitor with an EC50 of 80.8 µg/mL. Schirubridilactone D is a nortriterpenoid isolated from the leaves and stems of Schisandra rubriflora. Schirubridilactone D inhibits HIV-1 replication and blocks HIV-1-induced cytopathic effects. Schirubridilactone D is applicable to research related to HIV-1 infection.
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PD 161374
0 ImagesCat. No.: HY-106971CAS No.: 177785-47-6PD 161374 is an inhibitor targeting the HIV-1 nucleocapsid protein NCp7. PD 161374 primarily acts on the early stages of viral replication, inhibiting the completion of reverse transcription without affecting viral entry or later assembly. PD 161374 remains active against HIV-1, HIV-2, SIV, and drug-resistant strains. PD 161374 can be used to study antiretroviral agents.
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Stavudine sodium
0 ImagesSynonyms: d4T sodiumStavudine (d4T) sodium is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Stavudine sodium has activity against HIV-1 and HIV-2. Stavudine sodium also inhibits the replication of mitochondrial DNA (mtDNA). Stavudine sodium reduces NLRP3 inflammasome activation and modulates Amyloid-β autophagy. Stavudine sodium induces apoptosis.
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NNRT-IN-10
0 ImagesCat. No.: HY-174417CAS No.: 2459751-62-1NNRT-IN-10 is a potent, selective and orally active non-nucleoside HIV-1 reverse transcriptase (NNRTI) inhibitor with with an EC50 values ranging from 1.16 to 18.3 nM for HIV and its mutant strains. NNRT-IN-10 exhibits good pharmacokinetic properties and favorable safety profiles. NNRT-IN-10 can be used for the study of AIDS, caused by HIV-1.
