bpr

Bromophenol red (BPR) is a chemical indicator. It has been shown to bind to lysozymes and inhibits their activity against bacterial cell walls, but not against the polysaccharide component of peptidoglycan.

BPR0L075 [6-methoxy-3-(3',4',5'-trimethoxy-benzoyl)-1H-indole] is an antitubulin compound with anticancer properties and demonstrates antimitotic activity.

BPR1M97 is a mu opioid receptor (MOP) and neuropeptide-orphin FQ (NOP) receptor agonist with blood-brain barrier permeability and potency, with Kis values of 1.8 nM for MOP and 4.2 nM for NOP.BPR1M97 exhibits anti-injurious effects and antinociceptive effects.

DBPR112 is an orally active furanopyrimidine-based EGFR inhibitor with IC50s of 15 nM for EGFRWT and 48 nM for EGFRL858R T790M, capable of occupying the ATP-binding site and demonstrating significant antitumor efficacy.

DBPR108 is an orally bioavailable dipeptide-derived DPP4 inhibitor (IC50: 15 nM) and it has no inhibition on DDP8 and DPP9.

BPR1J-097) is a novel FLT-3 inhibitor(IC50: 11±7 nM) with promising in vivo anti-tumor activities. It also inhibits FLT-3 D835Y (IC50: 3 nM).

BPR1R024 is an orally active and selective CSF1R inhibitor with an IC50 of 0.53 nM.

BPR1J-097, a new-type small molecule FLT-3 inhibitor(IC50=11±7 nM), is with great anti-tumor activities in vivo.

BPR1K871, a preclinical development candidate for anti-cancer therapy [1], is a potent, selective dual inhibitor targeting FLT3 and AURKA, with IC50 values of 19 nM and 22 nM, respectively.

DBPR-110 is a nonstructural protein 5A (NS5A) inhibitor. DBPR-110 reduced the reporter expression of the HCV1b replicon with a EC(50) and a selective index value of 3.9 ± 0.9 pM and >12,800,000, respectively. DBPR-110 reduced HCV2a replicon activity with

BPRMU191 is a distinct mu-opioid receptor (MOR) modulator with an EC50 of 2.17 μM in FLIPR Ca2+ assays conducted on CHO-K1 MOR Gα15 cells. Additionally, BPRMU191 interacts with MOR in the presence of naloxone.

BPR3P0128, a non-nucleoside RNA-dependent RNA polymerase (RdRp) inhibitor, is effective orally and can inhibit various SARS-CoV-2 variants. It exhibits EC 50 values of 0.62 µM for SARS-CoV-2 and 0.14 µM for HCoV-229E, demonstrating potent anti-pancoronavirus activity at submicromolar concentrations. Additionally, BPR3P0128 displays synergistic antiviral effects when used in combination with Remdesivir [1].

BPR5K230 is a dual inhibitor of the receptor tyrosine kinases MER and AXL, exhibiting IC50 values of 4.1 nM and 9.2 nM, respectively. It inhibits the proliferation of Ba F3-MER cells with an IC50 of 5 nM. BPR5K230 demonstrates favorable pharmacokinetics in mice and displays anti-inflammatory and antitumor effects in mouse models against 4T1, MDA-MB-231, MC38, and Hepa1-6.

DBPR112 is a potent EGFR inhibitor (IC50=487 nM) as a Clinical Candidate for the Treatment of Non-Small Cell Lung Cancer. DBPR112), DBPR112 not only displayed a potent inhibitory activity against EGFRL858R T790M double mutations but also exhibited tenfold potency better than the third-generation inhibitor, osimertinib,against EGFR and HER2 exon 20 insertion mutations. Overall, pharmacokinetic improvement through lead-to-candidate optimization yielded fourfold oral AUC better that afatinib along with F = 41.5%, an encouraging safety profile, and significant antitumor efficacy in in vivo xenograft models.

BPR1J-340 is a potent and selective FLT3 inhibitor with potential anticancer activity. BPR1J-340 was identified as a novel potent FLT3 inhibitor by biochemical kinase activity (IC50 approximately 25 nM) and cellular proliferation (GC50 approximately 5 nM) assays. BPR1J-340 inhibited the phosphorylation of FLT3 and STAT5 and triggered apoptosis in FLT3-ITD(+) AML cells. The pharmacokinetic parameters of BPR1J-340 in rats were determined. BPR1J-340 also demonstrated pronounced tumor growth inhibition and regression in FLT3-ITD(+) AML murine xenograft models. The combination treatment of the HDAC inhibitor vorinostat (SAHA) with BPR1J-340 synergistically induced apoptosis via Mcl-1 down-regulation in MOLM-13 AML cells, indicating that the combination of selective FLT3 kinase inhibitors and HDAC inhibitors could exhibit clinical benefit in AML therapy.

IBPR002 is an aurora kinase inhibitor which reveals mechanisms of HURP in nucleation of centrosomal and kinetochore microtubules.

BPR1K653 is a potent Aurora kinase inhibitor with potential anticancder activity. BPR1K653 specifically inhibited the activity of Aurora-A and Aurora-B kinase at low nano-molar concentrations in vitro. BPR1K653 was potent in targeting a variety of cancer cell lines regardless of the tissue origin, p53 status, or expression of MDR1. At the cellular level, BPR1K653 induced endo-replication and subsequent apoptosis in both MDR1-negative and MDR1-positive cancer cells. Importantly, it showed potent activity against the growth of xenograft tumors of the human cervical carcinoma KB and KB-derived MDR1-positive KB-VIN10 cells in nude mice. Finally, BPR1K653 also exhibited favorable pharmacokinetic properties in rats., BPR1K653 is a promising anti-cancer compound that has potential for the management of various malignancies, particularly for patients with MDR1-related drug resistance after prolonged chemotherapeutic treatments.

DBPR116 is a prodrug of BPRMU191 that can penetrate the blood-brain barrier. It significantly enhances the delivery efficiency of drugs targeting the central nervous system. When combined with the antagonist Naltrexone, DBPR116 demonstrates superior safety and analgesic effects compared to morphine in various in vivo pharmacological studies, including thermal pain models, cancer pain models, constipation, sedation, psychological dependence, heart rate, and respiratory frequency. As a strategy for peripheral administration, DBPR116 effectively alleviates pain while reducing adverse effects, showing promise as a safer opioid analgesic.

Uk-390957 is a sulfonamide compound with a high BPR due to binding to carbonic anhydrase.

FPL-63012AR is a D1-receptor agonist.