Olacaftor is a CFTR modulator for cystic fibrosis research
**Background**
Cystic fibrosis (CF) is a severe genetic disorder caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR protein functions as a chloride channel across the epithelial cell membranes of various organs, including the lungs and pancreas. When the CFTR protein is dysfunctional or absent, it leads to the production of thick, sticky mucus, resulting in chronic pulmonary infections, progressive lung damage, and multi-organ failure. Developing small molecules that can correct the folding of the CFTR protein or potentiate its gating activity is a critical strategy for treating this disease. In this context, we will introduce a CFTR modulator – Olacaftor.
**Definition**
Olacaftor (VX-440) is a cystic fibrosis transmembrane conductance regulator (CFTR) modulator. According to the Olacaftor description, this compound is designed to improve the function of the CFTR protein to alleviate the symptoms associated with cystic fibrosis.
**Mechanism of Action**
Olacaftor acts as a modulator of the CFTR channel, aiming to restore the transport of chloride ions across the cell membrane. By improving the stability and gating of the CFTR protein, it helps normalize the viscosity of mucus in the respiratory tract. Researchers seeking detailed Olacaftor technical information can refer to its chemical properties, including its molecular weight of 539.66 and its Olacaftor Formula, $\text{C}_{29}\text{H}_{34}\text{FN}_3\text{O}_4\text{S}$.
**Experimental Studies**
The Olacaftor biological activity has been characterized through extensive pharmacological evaluations. As detailed in the Olacaftor References, the compound was developed to target specific CFTR mutations to enhance protein trafficking and function. While specific IC50 values and detailed cell line concentrations are typically proprietary or specified in the patent documentation, the compound has been validated for its ability to modulate the CFTR protein. In conclusion, Olacaftor is a potent CFTR modulator that holds significant potential for the treatment of cystic fibrosis.
Keywords
Olacaftor, 1897384-89-2, VX-440, VX440, VX 440, CFTR, Autophagy, Cystic fibrosis transmembrane conductance regulator, Inhibitor, inhibitor, inhibit
References
[1] Miller M, et al. Modulators of cystic fibrosis transmembrane conductance regulator. US9782408.
A 51-year-old woman was diagnosed with essential thrombocythemia (ET) in 1995, presenting with a markedly elevated platelet count of 1240 × 10⁹/L and hypercellular bone marrow dominated by large, mature megakaryocytes. Over the next 16 years, she remained stable on anti-thrombotic therapy, with no evidence of thrombosis or progression to myelofibrosis. In October 2011, at age 67, she presented with progressive cytopenia and an abrupt decline in platelets to 336 × 10⁹/L, accompanied by 14% blasts in peripheral blood. Bone marrow examination revealed hypercellularity with 76% leukemic blasts and increased megakaryocytes. Immunophenotyping confirmed a B-cell lineage phenotype (CD34+ CD19+ CD10+ HLA-DR+), and molecular analysis demonstrated monoclonal immunoglobulin heavy chain rearrangement. Cytogenetic and FISH studies identified the Philadelphia chromosome translocation t(9;22)(q34;q11.2) and monosomy 7. RT-PCR detected the minor BCR-ABL1 fusion transcript, confirming the diagnosis of Ph+ALL.
To determine clonal origins, mutational analysis was performed on granulocytes, lineage-negative CD34+ hematopoietic stem and progenitor cells (HSPCs), and CD34+CD19+ B-ALL cells.6-(4-Hydroxyphenoxy)hexyl custom synthesis JAK2-V617F mutation was present in granulocytes and HSPCs but absent in the B-ALL population, indicating that the Ph+ALL clone did not originate from the JAK2-mutated ET clone.Arterolane Activator Further investigation into the timing of BCR-ABL1 acquisition revealed that the minor transcript was detectable not only in committed B-cell precursors (CD34+CD19+CD10+) but also in the CD34+CD19−CD10− HSPC-enriched population, suggesting early acquisition prior to B-cell commitment.PMID:35228900 FISH confirmed the presence of the Philadelphia chromosome in 54% of CD34+CD19−CD10− cells and 10% of granulocytes.
The patient was treated with dasatinib and prednisolone. Four weeks later, blast counts declined significantly. However, RT-PCR analysis of sorted bone marrow subpopulations showed rapid disappearance of the minor BCR-ABL1 transcript in CD34+CD19− cells—likely representing primitive HSPCs—but persistence in CD34+CD19+ cells. Despite this, the transcript remained detectable at low levels in bulk bone marrow after ten weeks. Nine months post-treatment initiation, relapse occurred with the emergence of the T315I mutation, indicating selection of a resistant clone within the committed B-cell compartment rather than from the most primitive stem cells.
This case highlights the complexity of clonal evolution in MPN-associated leukemias. The absence of JAK2-V617F in Ph+ALL cells demonstrates that transformation to lymphoid leukemia can occur independently of the MPN clone. Moreover, the persistence of BCR-ABL1 in committed B-cells despite clearance in HSPCs challenges the assumption that resistance arises solely from quiescent stem cells. These findings suggest that the resistant clone may reside in differentiated populations, possibly due to microenvironmental protection or intrinsic resistance mechanisms. This observation bridges gaps between murine models and human disease, underscoring the need for deeper investigation into the biology of resistant clones in Ph+ALL patients undergoing TKI therapy.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com
Natural antisense transcripts (NATs) represent a significant class of regulatory RNAs that exhibit sequence complementarity to other transcripts. These molecules are increasingly recognized for their roles in post-transcriptional gene regulation across eukaryotes, including plants. In soybean (Glycine max), NATs have been predicted in the PlantNATsDB, yet comprehensive functional and structural analyses remain limited. This study presents a large-scale prediction and experimental validation of NATs in soybean, integrating high-throughput sequencing data from small RNAs and degradome profiles. A total of 26,216 NATs were identified, comprising 994 cis-NATs and 25,222 trans-NATs. Each sense transcript was found to associate with between one and 177 antisense transcripts, highlighting the complexity of NAT interactions. RT-PCR amplification confirmed the expression of 21 trans-NATs, providing direct evidence of their biological relevance.
Further analysis revealed that 179 cis-NATs and 6,629 trans-NATs produce small RNAs, predominantly enriched within overlapping regions. The most abundant small RNA species were 21, 22, and 24 nucleotides in length—consistent with typical sizes of natural antisense siRNAs (nat-siRNAs). The generation of these small RNAs showed a strong bias toward one strand of the NAT duplex, suggesting directional processing by Dicer-like enzymes. Degradome sequencing enabled global identification of nat-siRNA targets, revealing 446 target genes associated with 165 distinct nat-siRNAs. Notably, these targets included not only the sense or antisense strands of the originating NAT but also unrelated transcripts, indicating broad regulatory potential. Five NAT transcripts were found to form stem-loop structures characteristic of pre-microRNAs, suggesting dual functionality in both miRNA and nat-siRNA biogenesis. Additionally, 86 known miRNA targets were identified as having antisense transcripts, implying cross-talk between miRNA and NAT pathways.5-TAMRA Cadaverine In stock
These findings collectively demonstrate that NATs in soybean function within intricate regulatory networks involving small RNAs, transcriptional interference, and post-transcriptional silencing.N-Boc-7-aminoheptanoic acid medchemexpress The interplay among cis- and trans-NATs, nat-siRNAs, miRNAs, and their respective targets suggests a highly coordinated system influencing gene expression during development and stress responses.PMID:35247502 This work provides a foundational resource for understanding the regulatory landscape of soybean, offering insights into how non-coding RNAs shape genome activity and adaptation.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com
**Background**
Heat shock protein 90 (Hsp90) is a highly conserved molecular chaperone that plays a critical role in maintaining the stability and function of numerous client proteins, many of which are oncogenic kinases and transcription factors. Due to its ability to facilitate the folding and maturation of proteins essential for cell survival and proliferation, Hsp90 is frequently overexpressed in various malignancies. Inhibiting Hsp90 leads to the degradation of these client proteins, thereby suppressing tumor growth and inducing apoptosis. Consequently, Hsp90 has become a primary therapeutic target in the development of anticancer strategies. In this context, we will introduce an Hsp90 C-terminal inhibitor – HSP90-IN-22.
**Definition**
HSP90-IN-22 (Compound 35) is a potent Hsp90 inhibitor that exhibits significant antiproliferative properties against human breast cancer cell lines.
**In Vitro Studies**
Regarding the HSP90-IN-22 description, this compound is a 6-acylamino-2-aminoquinoline derivative with a molecular weight of 434.53 and the chemical formula C25H30N4O3. In terms of HSP90-IN-22 biological activity, the compound has been evaluated for its cytotoxicity using MTT assays. In vitro studies demonstrated that HSP90-IN-22 possesses potent antiproliferative activity against human breast cancer cells after 72 hours of incubation. Specifically, it exhibited IC50 values of 3.65 μM for MCF7 breast cancer cells and 2.71 μM for SKBr3 breast cancer cells. These results indicate that the compound effectively inhibits the proliferation of different breast cancer subtypes by targeting the Hsp90 pathway. In conclusion, HSP90-IN-22 is a novel Hsp90 C-terminal inhibitor with promising potential for breast cancer research.
Keywords
HSP90-IN-22, 442898-75-1, HSP, Heat shock proteins, MCF7 cells, SKBr3 cells, antiproliferative, Hsp90, Inhibitor, inhibitor, inhibit
References
Hyaluronic acid (HA) has emerged as a cornerstone in regenerative medicine due to its exceptional biocompatibility, biodegradability, and intrinsic bioactivity. As a major component of the extracellular matrix (ECM), HA plays a pivotal role in maintaining tissue hydration, structural integrity, and cellular signaling. In the context of endometrial regeneration, HA-based hydrogels serve not only as physical barriers to prevent post-surgical adhesions but also as dynamic delivery systems capable of sustained release of therapeutic agents. These hydrogels are particularly advantageous because they mimic the natural ECM environment, supporting cell attachment, migration, and proliferation while modulating inflammatory responses.
Recent studies have demonstrated that HA hydrogels can significantly reduce the incidence of intrauterine adhesions (IUA) following hysteroscopic procedures. Clinical meta-analyses indicate that HA gel application is especially effective in preventing moderate-severity adhesions and improving uterine receptivity, particularly in patients undergoing assisted reproductive technologies like IVF. However, its efficacy diminishes in severe cases, where additional therapeutic support is required. To overcome this limitation, researchers have developed advanced formulations incorporating bioactive molecules such as stem cell secretomes, growth factors, and hormones.
One notable innovation involves the integration of mesenchymal stem cell-secretome (MSC-Sec) into HA hydrogels. Liu et al. engineered a stem cell-secretome-modified HA hydrogel that enhances the localized delivery of key regenerative factors including epidermal growth factor (EGF), fibroblast growth factor (FGF), insulin-like growth factor-1 (IGF-1), and IGF-binding protein (IGFBP). This system prolongs the retention time of secreted proteins within the uterine cavity, resulting in thicker endometrial layers and increased glandular density compared to HA alone. The nano-scale architecture of these scaffolds enables controlled release and facilitates intercellular communication via extracellular vesicles, thereby promoting functional tissue recovery.
Another promising approach is the use of decidualized endometrial stromal cells (dEMSCs) encapsulated in HA hydrogels. Kim et al. reported that dEMSC-loaded HA hydrogels accelerated endometrial regeneration in murine models, reducing fibrotic tissue formation and restoring expression of implantation-related markers such as Desmin, CD44, PECAM, and IGF-1. Importantly, embryos transferred into treated animals successfully implanted and developed into live offspring, demonstrating functional recovery of the uterus.
The versatility of HA extends beyond simple carrier functions. Its ability to be chemically modified through click chemistry or supramolecular interactions allows for the design of stimuli-responsive hydrogels that respond to temperature, pH, or enzymatic activity.6-Aminoindole Autophagy These smart materials can be tailored for spatiotemporal control over drug release, enhancing therapeutic precision.1,8-Diaminooctane custom synthesis Moreover, HA’s susceptibility to degradation by hyaluronidases ensures gradual clearance, minimizing long-term foreign body reactions.PMID:34896311
In summary, HA-based hydrogels represent a highly adaptable and effective platform for endometrial regeneration. By combining mechanical support with biological functionality—delivering stem cells, growth factors, and immune-modulating signals—they address multiple aspects of tissue repair. Future developments will focus on optimizing crosslinking density, integrating multi-agent delivery systems, and advancing clinical translation to improve outcomes for women suffering from Asherman’s syndrome and endometrial atrophy.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com
**Background**
Autoinflammatory diseases are characterized by inappropriate activation of the innate immune system, leading to systemic inflammation and tissue damage. Interleukin-18 (IL-18) is a potent pro-inflammatory cytokine that plays a critical role in the pathogenesis of various inflammatory conditions, including Adult-Onset Still’s Disease (AOSD) and atopic dermatitis. By triggering the production of interferon-gamma (IFN-γ) and other chemokines, IL-18 contributes to the chronic inflammatory cycle observed in these disorders. Consequently, targeting the IL-18 pathway has emerged as a promising therapeutic strategy to mitigate systemic inflammation and improve patient outcomes. In this context, we will introduce a fully human monoclonal antibody targeting IL-18 – Camoteskimab.
**Definition**
Camoteskimab is a fully human IgG1 kappa monoclonal antibody with high affinity for IL-18, exhibiting a binding affinity of 63 pM.
**In Vitro Studies**
According to the Camoteskimab description, this antibody is designed to neutralize the activity of IL-18 and inhibit the formation of the active IL-18/Ra/RB complex. In Camoteskimab In Vitro assays using PBMCs, the antibody potently neutralizes IL-18 activity with an IC50 in the sub-nanomolar range. Furthermore, the Camoteskimab biological activity has been validated through binding assays; immobilized human IL-18 protein binds to Camoteskimab with an EC50 of 201.8 ng/mL. Flow cytometric analysis using A431 cells further confirms its efficacy, where cells stained with the primary antibody at a 1/200 dilution showed significant binding compared to the Human IgG1 kappa isotype control. For researchers seeking detailed experimental parameters, the Camoteskimab protocol provides guidance on reconstitution using sterile PBS or saline. In conclusion, Camoteskimab is a high-affinity neutralizing antibody that serves as a powerful tool for studying the role of IL-18 in autoinflammatory diseases.
Keywords
Camoteskimab, 2492472-82-7, AVTX-007, CERC-007, MEDI 2338, AVTX007, AVTX 007, CERC007, CERC 007, MEDI2338, MEDI-2338, Interleukin Related, IL
References
[1] Bindoli S, et al. Adult-Onset Still’s Disease (AOSD): Advances in Understanding Pathophysiology, Genetics and Emerging Treatment Options. Drugs. 2024;84(3):257-274.
[2] Chen X, et al. Identification of cross-talk pathways and PANoptosis-related genes in periodontitis and Alzheimer’s disease by bioinformatics analysis and machine learning. Front Aging Neurosci. 2024 Aug 27;16:1430290.
[3] Richard Brown, et al. Anti-il-18 antibody therapy for treating atopic dermatitis. WO2024261470A1. 2025-12-20.
[4] Galozzi P, et al. Progress in Biological Therapies for Adult-Onset Still’s Disease. Biologics. 2022;16:21-34. Published 2022 Apr 21.
Chronic exposure to elevated manganese levels is increasingly recognized as a significant risk factor for neurocognitive and motor impairments, particularly in children. Despite this, the cellular mechanisms underlying manganese toxicity remain poorly understood, especially during the transition from physiological to toxic exposure levels. This study investigates Golgi Phosphoprotein 4 (GPP130) as a potential biomarker of manganese exposure in AF5 GABAergic neuronal cells, focusing on its specificity, sensitivity, and temporal dynamics. Our findings demonstrate that GPP130 degradation is highly specific to manganese among various divalent cations, including cobalt, copper, iron, nickel, and zinc, with no detectable degradation observed under any of these alternative exposures. Notably, GPP130 degradation occurs rapidly—within one hour of manganese exposure—and at remarkably low concentrations: as little as 0.54 µM Mn, which is approximately 200 times lower than previously reported thresholds. Crucially, this response occurs without measurable increases in intracellular manganese levels, indicating that GPP130 degradation is not a consequence of accumulated metal but rather an early signaling event in response to extracellular manganese flux.
Further analysis reveals that GPP130 degradation follows a biphasic pattern: initial rapid loss coincides with a transient spike in intracellular Mn, followed by a decline in both Mn levels and GPP130 protein over time, even under continued exposure. This suggests that GPP130 may play a regulatory role in manganese homeostasis, possibly facilitating efflux or redistribution. Recovery studies show that while GPP130 levels begin to rebound after cessation of exposure, recovery is slow and incomplete, underscoring the persistence of the cellular stress response.Neurogranin Proteinmedchemexpress In vivo validation in rats subchronically exposed to manganese via intraperitoneal injection (9.6 mg/kg/day, three times weekly for four weeks) confirms the relevance of these findings. Control animals exhibit GPP130 immunoreactivity in only 15–30% of striatal and cortical neurons, consistent with selective expression. After manganese exposure, there was a significant reduction in both the number of GPP130-positive cells and total protein levels across brain regions, confirming that GPP130 degradation is not limited to cell culture but reflects a real biological response in the intact nervous system.
These results establish GPP130 as a highly sensitive and specific cellular indicator of manganese exposure, capable of detecting perturbations at physiologically relevant levels.1,4-Dibromo-2,5-diiodobenzene site Its rapid, Mn-specific degradation provides insight into early molecular events in manganese neurotoxicity and supports a potential role in cellular manganese regulation.PMID:35094932 Given that GPP130 is involved in endosome-to-Golgi trafficking, its disruption may impair critical protein sorting pathways, contributing to functional deficits. Moreover, the observation that some neurons maintain GPP130 despite exposure suggests differential susceptibility across cell populations, potentially explaining regional vulnerability in manganese-induced neurotoxicity. These findings highlight GPP130 as a promising target for monitoring environmental manganese exposure and understanding early mechanisms of brain injury.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com
**Background**
The G protein-coupled receptor 84 (GPR84) is a receptor primarily expressed in immune cells and is activated by medium-chain fatty acids. Activation of GPR84 plays a critical role in modulating inflammatory responses and the production of pro-inflammatory cytokines, such as interleukin-12 (IL-12). In the context of oncology, the modulation of the immune microenvironment is a key strategy for enhancing the efficacy of cancer therapies. Recent studies have highlighted the potential of GPR84 activation to trigger potent anti-tumor immune responses, making it an attractive target for treating various malignancies. Therefore, in this context, we will introduce a potent GPR84 activator – 3-Hydroxydodecanoic acid.
**Definition**
3-Hydroxydodecanoic acid is a medium-chain fatty acid and human endogenous metabolite that acts as an agonist of GPR84, exhibiting an EC50 value of 1.31 μM for the inhibition of forskolin-stimulated cAMP accumulation in CHO cells.
**In Vitro and In Vivo Studies**
According to the 3-Hydroxydodecanoic acid description, this compound serves as a powerful tool for studying immune-mediated tumor suppression. In vitro, 3-Hydroxydodecanoic acid (1-100 μM; 1 h) has been shown to induce lipid peroxidation in the rat cerebral cortex, resulting in increased TBA-RS levels. Furthermore, agonist activity was confirmed in CHO cell membranes co-expressing human GPR84 and beta-arrestin2, with an EC50 of 1.31 μM for cAMP inhibition and 3.25 μM for beta-arrestin 2 recruitment.
Regarding 3-Hydroxydodecanoic acid in vivo activity, the compound demonstrates significant anti-tumor effects in C57BL/6JRj mice bearing MC38 tumors. When administered via intraperitoneal injection (i.p.) on days 6, 9, and 12, it significantly reduced tumor growth. This effect was dependent on GPR84 receptor signaling and was characterized by increased IL-12 production and higher infiltration of CD8+ T cells within the tumors. Additionally, 3-Hydroxydodecanoic acid showed a strong synergistic anti-tumor effect when combined with 5-FU. These findings suggest that 3-Hydroxydodecanoic acid cancer research applications could extend to colon cancer, lung cancer, and melanoma. In conclusion, 3-Hydroxydodecanoic acid is a GPR84 agonist that promotes anti-tumor immunity via IL-12 production and T cell infiltration.
Keywords
3-Hydroxydodecanoic acid, 1883-13-2, Endogenous Metabolite, colon cancer, lung cancer, and melanoma, anticancer, mice., Inhibitor, inhibitor, inhibit
References
[1] Tonin AM, et al. Long-chain 3-hydroxy fatty acids accumulating in LCHAD and MTP deficiencies induce oxidative stress in rat brain. Neurochem Int. 2010 Jul;56(8):930-6.
[2] Katkeviciute E, et al. Bacteria-derived 3-hydroxydodecanoic acid induces a potent anti-tumor immune response via the GPR84 receptor. Cell Rep. 2025 Feb 26;44(3):115357.
**Background**
Obesity is a complex, chronic disease characterized by excessive adipose tissue accumulation, which significantly increases the risk of cardiovascular diseases, type 2 diabetes, and metabolic syndrome. The management of obesity often requires pharmacological interventions that target the central nervous system (CNS) to regulate appetite and energy expenditure. Monoamine neurotransmitters, including dopamine, norepinephrine, and serotonin, play critical roles in the modulation of food intake and satiety. Consequently, agents capable of modulating the synaptic levels of these neurotransmitters have become primary targets for the development of anti-obesity therapies. In this context, we will introduce a CNS-acting anti-obesity agent – Tesofensine.
**Definition**
Tesofensine (NS-2330) is a potent triple monoamine reuptake inhibitor that induces inhibition of the re-uptake process in the synaptic cleft for dopamine (IC50 = 6.5 nM), norepinephrine (IC50 = 1.7 nM), and serotonin (IC50 = 11 nM).
**In Vivo Studies**
According to the Tesofensine biological activity reported in literature, this compound demonstrates significant appetite-suppressing effects. In vivo studies using diet-induced obesity (DIO) rats showed that a single subcutaneous (s.c.) dose of Tesofensine (0.1-3 mg/kg) robustly and dose-dependently inhibits food intake over a 12-hour nocturnal observation period. The threshold dose for the inhibition of total food intake was found to be 1.0 mg/kg, with an estimated ED50 of 1.3 mg/kg. Furthermore, the Tesofensine protocol for chronic treatment involved daily subcutaneous administration of a moderate dose (2.0 mg/kg) over 16 days. This regimen triggered a significant reduction in body weight starting after 4 days of administration relative to vehicle-treated controls. Over the entire treatment period, the average relative decrease in body weight of treated DIO rats was 8.6±1.4%, representing a relative weight loss of 13.8±1.4% compared to the control group. In conclusion, Tesofensine is a potent triple monoamine reuptake inhibitor that effectively induces hypophagia and weight loss in obese animal models.
Keywords
Tesofensine, 195875-84-4, NS-2330, NS2330, NS 2330, Dopamine Transporter, Serotonin Transporter, DAT, SLC6A3, 5-HTT, SERT, SLC6A4, triple monoamine reuptake, neurotransmitters dopamine, norepinephrine, serotonin, anti-obesity agent, Inhibitor, inhibitor, inhibit
References
[1] Lieuwe Appel, et al. Tesofensine, a novel triple monoamine re-uptake inhibitor with anti-obesity effects: dopamine transporter occupancy as measured by PET. Eur Neuropsychopharmacol. 2014 Feb;24(2):251-61.
[2] Ann A Coulter, et al. Centrally Acting Agents for Obesity: Past, Present, and Future. Drugs. 2018 Jul;78(11):1113-1132.
[3] Anne Marie D Axel, et al. Tesofensine, a novel triple monoamine reuptake inhibitor, induces appetite suppression by indirect stimulation of alpha1 adrenoceptor and dopamine D1 receptor pathways in the diet-induced obese rat.Neuropsychopharmacology. 2010 Jun;35(7):1464-76.
**Background**
Fluorescent labeling is a fundamental tool in biomedical research, enabling the visualization and tracking of biomolecules within complex biological systems. Among various labeling strategies, bioorthogonal chemistry has emerged as a powerful approach, allowing for the selective modification of molecules in vivo or in vitro without interfering with native biological processes. Specifically, the azide-alkyne cycloaddition, often referred to as “click chemistry,” provides a highly efficient and stable method for attaching fluorophores to target proteins, lipids, or nucleic acids. This technology is particularly valuable in the development of functionalized nanobodies and the study of protein-protein interactions. In this context, we will introduce a potent fluorescent dye for these applications – Cyanine5 azide.
**Definition**
Cyanine5 azide is a fluorescent dye containing an azide group, characterized by an excitation wavelength ($\lambda_{ex}$) of 647 nm and an emission wavelength ($\lambda_{em}$) of 668 nm.
**Mechanism of Action**
According to the Cyanine5 azide description, this compound is designed for versatile conjugation via click chemistry. It contains a reactive azide group that can undergo a copper-catalyzed azide-alkyne cycloaddition (CuAAC) when reacted with terminal alkynes. Additionally, it can participate in ring strain-promoted alkyne-azide cycloaddition (SPAAC) with molecules containing dibenzocyclooctyne (DBCO) or bicyclo[6.1.0]nonyne (BCN) groups. This dual reactivity allows researchers to choose between copper-dependent and copper-free labeling methods depending on the sensitivity of their biological sample. For those seeking detailed Cyanine5 azide technical information, the compound possesses a molecular weight of 601.22 and a chemical formula of $\text{C}_{35}\text{H}_{45}\text{ClN}_6\text{O}$.
**Experimental Applications**
The utility of Cyanine5 azide has been demonstrated in advanced chemical synthesis and biological labeling. In studies regarding the total chemical synthesis of a functionalized GFP nanobody, the dye was employed to introduce fluorescence into the protein structure. When evaluating Cyanine5 azide in vitro, the dye’s strong emission in the far-red spectrum (662-668 nm) ensures minimal background interference and high signal-to-noise ratios in imaging experiments. The ability to precisely label nanobodies allows for the detailed study of target recognition and binding kinetics. In conclusion, Cyanine5 azide is a potent and versatile fluorescent probe for bioorthogonal labeling and imaging research.
Keywords
Cyanine5 azide, 1267539-32-1, Fluorescent Dye, fluorescent dye, copper-catalyzed click reaction, azide, NIR live organism imaging, Inhibitor, inhibitor, inhibit
References