d-3

D-3 (phosphorpeptide) is an efficient, simple, and specific agent for eliminating iPSCs.

Dopamine D3 receptor agonist 13a selectively targets the dopamine D3 receptor over dopamine D1, D2, and D4 receptors, with affinities (Ki values) of 0.14, 4,600, 2.85, and 756 nM, respectively. It also interacts with serotonin (5-HT) receptor subtypes 5-HT1A, 5-HT2A, 5-HT2B, and 5-HT2C, with Ki values of 6, 54, 1.47, and 252 nM, respectively. While acting as a partial agonist at dopamine D2 receptors (EC50 = 2.26 nM in a G protein recruitment assay), it serves as an antagonist at dopamine D3 receptors (IC50 = 4.62 nM). Additionally, Dopamine D3 receptor agonist 13a, at a dose of 3 mg/kg, has been shown to reduce cocaine self-administration in rats.

APY-d3 is an EphA4-LBD antagonist peptide with a Kd value of 138 nM. It is constrained in a biologically active β-hairpin conformation through a disulfide bond linking its ends. APY-d3 is applicable for research in cancers such as gastric and pancreatic cancer, as well as in neurodegenerative diseases like amyotrophic lateral sclerosis and Alzheimer's disease.

Fmoc-D-3-Pal-OH is a useful organic compound for research related to life sciences. The catalog number is T65472 and the CAS number is 142994-45-4.

Desamino(D-3-(3′-pyridyl)-Ala2,Arg8)-Vasopressin, a synthetic analog of vasopressin (AVP), functions as a weak agonist at the antidiuretic receptor and a potent agonist at the pituitary corticotrope receptor [1].

(R)-2-((((9H-Fluoren-9-yl)methoxy)carbonyl)amino)-3,3-diphenylpropanoic acid is a useful organic compound for research related to life sciences. The catalog number is T65888 and the CAS number is 189937-46-0.

Human β-defensin-3 (HβD-3) is an antibiotic antimicrobial peptide synthesized by epithelial cells. It exhibits potent antimicrobial properties, mitigates inflammatory cytokine responses, and targets various microorganisms with IC90 values ranging from 6 to 25 μg/ml.

β-Amyloid (31-35) (β-Amyloid 31-35) is the shortest sequence of native Amyloid-β peptide.

CD31, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), is a receptor on endothelial cells for clostridium perfringens beta-Toxin (CPB). It also functions as an ER-MP12 antigen and connects mechanical stress, metabolism, and inflammation. The CD31 peptide promotes phosphorylation of CD31 ITIM 686 and SHP2, thereby inhibiting TCR-induced T-cell activation [1]-[5].

CD31 TFA, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), functions as the specific receptor for Clostridium perfringens beta-Toxin (CPB) in endothelial cells. It is recognized as an ER-MP12 antigen and plays a pivotal role in connecting mechanical stress, metabolism, and inflammation. Additionally, the CD31 TFA peptide facilitates the phosphorylation of CD31 ITIM 686 and SHP2, further inhibiting TCR-induced T-cell activation [1]-[5].

Myr-TAT-CBD3, a CRMP2-CaV2.2 interaction inhibitor, has been shown to significantly attenuate carrageenan-induced thermal hypersensitivity and reverse thermal hypersensitivity in a rat model of postoperative pain, making it a useful compound for studying inflammation and postoperative pain [1].

Thrombospondin-1 (TSP-1)-derived CD36 binding motif is a bioactive peptide cyclized by a disulfide bond, critical for TSP-1-CD36 interaction. Involved in cancer metastasis, tumor adhesion, and angiogenesis, this matrix-bound glycoprotein-origin peptide competitively inhibits platelet aggregation and tumor metastasis.

PhD3, an antimicrobial peptide originating from monkey leukocytes, exhibits potent activity against various bacteria and the fungus Candida albicans [1].

Tat-CBD3 is a chemical compound inhibiting the interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2), as well as the interaction between CRMP2 and the NMDA receptor NR2B subunit. At a concentration of 10 µM, Tat-CBD3 reduces the Cav2.2-CRMP2 interaction by 43% in cell-free assays and impedes the NMDA receptor NR2B subunit-CRMP2 interaction in immunoprecipitation assays. It lowers voltage-induced calcium currents by about 60% in primary rat dorsal root ganglion (DRG) neurons and decreases glutamate-induced cytosolic calcium level rises in primary rat hippocampal neurons. When administered at 20 mg/kg, Tat-CBD3 lessens infarct volume in a rat model of cerebral ischemia following middle cerebral artery occlusion (MCAO). Additionally, intrathecal delivery of Tat-CBD3 at a dose of 20 µg/5 µl mitigates carrageenan-induced thermal hypersensitivity in rats.

Tat-CBD3A6K, a peptide derivative of the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2) interaction inhibitor Tat-CBD3, has demonstrated efficacy in a rat model of antiretroviral neuropathic pain caused by stavudine (d4T). Administered at 10 mg/kg, it preserves paw withdrawal threshold, indicating pain relief, and reduces the number of action potentials in dorsal root ganglia (DRG) neurons from affected rats. Additionally, a 30 µM/animal dural dose of Tat-CBD3A6K lessens meningeal blood flow escalation triggered by capsaicin, showcasing its potential in managing neuropathic pain and inflammation.

Myr-Tat-CBD3 is a chemical compound that serves as an inhibitor of the protein-protein interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2). This compound effectively disrupts the Cav2.2-CRMP2 interaction by about 81% at a 10 µM concentration and demonstrates an inhibitory concentration 50 (IC50) value of approximately 2.8 µM against potassium-induced calcium influx in primary rat dorsal root ganglion (DRG) neurons. Furthermore, at a concentration of 20 µM, Myr-Tat-CBD3 specifically inhibits calcium currents without affecting sodium currents in primary DRG neurons. Additionally, intrathecal administration of 20 µg/5 µl of Myr-Tat-CBD3 effectively mitigates carrageenan-induced declines in paw withdrawal latencies in rats, indicating its potential for pain relief. The compound also notably reduces cue-induced reinstatement of cocaine-seeking behavior in rats, suggesting therapeutic potential in addiction treatment.

6-Hydroxy Buspirone, an active metabolite of the anxiolytic compound buspirone, is produced via the cytochrome P450 (CYP) isoform CYP3A4. This compound exhibits affinity for the serotonin (5-HT) receptor subtype 5-HT1A, demonstrating efficacy in the rat hippocampus and dorsal raphe with half-maximal effective concentrations (EC50s) of 4 and 1 µM, respectively. Furthermore, 6-Hydroxy Buspirone acts as a potent antagonist against dopamine D2, D3, and D4 receptors with half-maximal inhibitory concentrations (IC50s) of 3.1, 4.9, and 0.85 µM, respectively, and inhibits the organic cation transporters 1 (OCT1), OCT2, and OCT3 in S2 proximal tubule cells expressing human transporters, showcasing a concentration-dependent mechanism.

β-Amyloid (35-42), a peptide derived from the beta-amyloid protein, encompasses amino acids 35 through 42.

β-Amyloid (33-40) is a peptide composed of amino acids 33 to 40 from the beta-amyloid protein.

Noraramtide (BHV-1100) is an antibody recruiting molecule that specifically binds to the CD38 molecule to recruit natural killer (NK) cells. This interaction enhances the NK cells' ability to kill tumor cells through antibody-dependent cellular cytotoxicity (ADCC). This mechanism allows NK cells to more effectively recognize and eliminate tumor cells while preventing mutual NK cell destruction. Noraramtide is utilized in research on autologous cancer immunotherapy.

TAT-CBD3, a 15-amino acid peptide derived from CRMP2, is fused with the TAT cell-penetrating sequence from the HIV-1 protein. It disrupts the CRMP2-NMDAR interaction without altering NMDAR localization.

TAT-CBD3A6K is a modified TAT-CBD3 peptide. It reduces T-type and R-type voltage-dependent calcium currents in dorsal root ganglion (DRG) neurons. By inhibiting CRMP-2-mediated enhancement of T-type and R-type calcium channel function, TAT-CBD3A6K exhibits anti-nociceptive effects in models of AIDS-induced peripheral neuropathy.

N'-Nitro-D-arginine (N'-Nitro-D-arginine) is a Building Block.

CREBtide acetate is a synthetic substrate for PKA (Km=3.9 μM), which is based on the phosphorylation sequence in d-CREB (cAMP response element binding protein).