Ro 08-2750

antagonist of nerve growth factor (NGF) CAS# 37854-59-4

Ro 08-2750

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Quality Control of Ro 08-2750

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Chemical structure

Ro 08-2750

3D structure

Chemical Properties of Ro 08-2750

Cas No. 37854-59-4 SDF Download SDF
PubChem ID 17756791 Appearance Powder
Formula C13H10N4O3 M.Wt 270.24
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 50 mM in 1eq. NaOH and to 10 mM in DMSO with gentle warming
Chemical Name 7,10-dimethyl-2,4-dioxobenzo[g]pteridine-8-carbaldehyde
SMILES CC1=CC2=C(C=C1C=O)N(C3=NC(=O)NC(=O)C3=N2)C
Standard InChIKey JDEMVNYMYPJJIM-UHFFFAOYSA-N
Standard InChI InChI=1S/C13H10N4O3/c1-6-3-8-9(4-7(6)5-18)17(2)11-10(14-8)12(19)16-13(20)15-11/h3-5H,1-2H3,(H,16,19,20)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Ro 08-2750

DescriptionNon-peptide inhibitor of NGF that binds the NGF dimer (KD ~ 1 μM) possibly causing a conformational change. Selectively inhibits binding of NGF to p75NTR at submicromolar concentrations, and to both p75NTR and TrkA at concentrations > 5 μM. Prevents NGF-induced apoptosis in SK-N-MC cells.

Ro 08-2750 Dilution Calculator

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Preparing Stock Solutions of Ro 08-2750

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.7004 mL 18.5021 mL 37.0041 mL 74.0083 mL 92.5104 mL
5 mM 0.7401 mL 3.7004 mL 7.4008 mL 14.8017 mL 18.5021 mL
10 mM 0.37 mL 1.8502 mL 3.7004 mL 7.4008 mL 9.251 mL
50 mM 0.074 mL 0.37 mL 0.7401 mL 1.4802 mL 1.8502 mL
100 mM 0.037 mL 0.185 mL 0.37 mL 0.7401 mL 0.9251 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Ro 08-2750

IC50: 1 μM (binds to NGF) [1]

Ro 08-2750 is an antagonist of nerve growth factor (NGF), which selectively inhibits binding to p75NTR over TRKA147. This selectivity was used to study the functions of p75NTR and TrkA in apoptosis, neuronal differentiation and neurite outgrowth. NGF is a neuropeptide mainly involved in the regulation of growth, proliferation, maintenance, and survival of certain target neurons.

In vitro: Ro 08-2750 can bind to the NGF dimer with ~ 1:1 binding ratio. Binding of Ro 08-2750 to NGF induces NGF a concentration-dependent conformational change [1]. Binding with low concentration of Ro 08-2750, NGF can no longer bind to p75NTR anymore, however, binding to TrkA is not impaired. At higher concentrations of Ro 08-2750 more than 5 mM, the NGF/Ro 08-2750 complex can not bind to TrkA as well. In SK-N-MC cells, Ro 08-2750 leads to inhibition of NGF-induced programmed cell death. In PC12 cells, Ro 08-2750 can enhance the signal pathway through TrkA[2].

In vivo:. So far, in vivo study has been conducted.

Clinical trial: So far, no clinical study has been conducted.

References:
[1] Arkin MR, Wells JA.  Small-molecule inhibitors of protein-protein interactions: progressing towards the dream. Nat Rev Drug Discov. 2004 Apr;3(4):301-17.
[2] Niederhauser O, Mangold M, Schubenel R, Kusznir EA, Schmidt D, Hertel C.  NGF ligand alters NGF signaling via p75(NTR) and trkA. J Neurosci Res. 2000 Aug 1;61(3):263-72.

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References on Ro 08-2750

Anti-La positive, anti-Ro negative subset of primary Sjogren's syndrome: anti-La is a reality but is the disease?[Pubmed:28229827]

Clin Exp Rheumatol. 2017 May-Jun;35(3):438-444. Epub 2017 Feb 20.

OBJECTIVES: To characterise the serological and clinical findings in primary Sjogren's syndrome in which anti-La was found without anti-Ro. We hypothesised that a significant portion of these are falsely negative for anti-Ro60. METHODS: Twenty-nine sera from primary Sjogren's syndrome patients were tested for antibodies directed against La and Ro. Anti-La was detected using bovine La treated with or without DNAase and RNAase to identify potential false positivity. Anti-Ro60 antibodies were detected using HEp-2000 substrate (in which cells are transfected with human Ro60) and HEp-2 substrate. Anti-Ro60 and Ro-52 were also tested by in vitro transcription/translation followed by immunoprecipitation assay. RESULTS: All 29 sera bound La, even after treatment with DNAase and RNAase. Of the 29 sera, 25 were unequivocally negative on HEp-2000 (1:40 dilution). Four samples were anti-Ro60 positive with a speckled pattern, three of the four at 1:320 dilution. Thus, false negative anti-Ro60 exists in a small fraction (14%) of the Ro-negative/La-positive primary Sjogren's patients. However, all the samples were negative for Ro60 and Ro52 by in vitro immunoprecipitation assay. Clinically these patients tended not to have salivary gland pathology characteristic of Sjogren's syndrome. CONCLUSIONS: We found only a small fraction of Ro negative/La positive sera to show positive HEp-2000 pattern. These subjects did not have characteristic findings on pathological examination of minor salivary glands, suggesting these subjects have a process distinct from Sjogren's syndrome.

Spontaneous Remission of Congenital Complete Atrioventricular Block in Anti-Ro/La Antibody-Negative Monozygotic Twins: Case Report.[Pubmed:28251027]

Balkan Med J. 2017 Jan;34(1):71-73.

BACKGROUND: Congenital complete atrioventricular block without any structural heart disease and anti-Ro/La negativity is very rare. Discordant complete atrioventricular block, which is more frequently defined in the literature as an autoimmune mechanism, is much more rare in monozygotic twins. CASE REPORT: The 26-year-old healthy mother had given birth in her first spontaneous, uneventful pregnancy to monozygotic twins at week 35. While the first twin's physical examination proved her to be normal with a pulse rate consistent with her age, the second twin had a pulse rate of approximately 40 beats/minute.The patient was confirmed to have congenital complete atrioventricular block. CONCLUSION: Despite this case appears to be an isolated one, a discordant complete atrioventricular block regression without any autoimmune evidence should be included in the differential diagnosis of bradycardia in infants.

Low titer, isolated anti Ro/SSA 60 kd antibodies is correlated with positive pregnancy outcomes in women at risk of congenital heart block.[Pubmed:28204891]

Clin Rheumatol. 2017 May;36(5):1155-1160.

Congenital heart block (CHB) is an autoantibody mediated disorder presumably caused by placental transmission of maternal autoantibodies to Ro/SSA 52 kd, p200, Ro/SSA 60 kd, La/SSB ribonucleoproteins. This study investigated the clinical significance of isolated anti-Ro/SSA 52 kd, anti-p200, anti-Ro/SSA 60 kd, and anti-La/SSB antibodies in positive pregnant patients. One hundred sixty-three pregnant women positive to anti-Ro/SSA 52 kd and/or anti-Ro/SSA 60 kd and/or anti-La/SSB antibodies were prospectively enrolled in the study. Anti-Ro52, anti-Ro60, anti-p200, and anti-La antibodies were assayed using home-made ELISA assays. Isolated antibody positivity was found in 25 women (15.3%), while multiple antibody positivity in 138 (84.7%). Twenty-four developed CHB, and the 139 had a favorable pregnancy outcome. The prevalence of isolated anti-Ro/SSA 60 kd antibodies was significantly higher (p < 0.046) as the prevalence of lower mean antibody titers (p < 0.0001) in the later group. Confirmation of these results by large-scale studies could lead clinicians to recommend less stringent fetal echocardiography monitoring in women with isolated anti-Ro/SSA 60 kd antibodies.

Neonatal lupus: Follow-up in infants with anti-SSA/Ro antibodies and review of the literature.[Pubmed:28212920]

Autoimmun Rev. 2017 Apr;16(4):427-432.

Neonatal Lupus Syndrome (NLS) is a distinct clinical entity caused by transplacental passage of maternal anti-SSA/Ro antibodies (Ab). Mothers may have systemic lupus erythematosus, Sjogren syndrome, or other connective tissue disease, or may be completely healthy at the time of giving birth. NLS includes several clinical manifestations: complete congenital heart block (CCHB) and cutaneous lupus are the most common, while hepatobiliary disease, hematological manifestations and central nervous system involvement may occur. Data from literature on the incidence of the different clinical manifestations of NLS are difficult to compare because they come mostly from retrospective studies or prospective studies, but up to date no systematic follow-up was carried out. We performed a large prospective single-center study with a systematic clinical and instrumental follow-up until 9months of life, in order to evaluate the incidence and the clinical impact of NLS features. From 2004 to 2014 all infants born in our center to mothers with anti-SSA/Ro Ab were enrolled in a specific diagnostic and follow-up (FU) program. At birth, 50 infants born to mothers with anti-SSA/Ro Ab were found positive for anti-SSA/Ro Ab. Infants were tested for anti SSA/Ro Ab at 3months of life, if positive they were re-tested at 6 and 9months. At 9months anti-SSA/Ro Ab were positive in 10% of children. In two cases (4%) a CCHB was identified during pregnancy and required pacemaker implantation at birth. In 10% of cases a transient ECG alterations was found during follow-up. Hematological NLS features (anemia, neutropenia, thrombocytopenia) were found at birth and during FU in several patients, in all cases without clinical manifestations and in most cases with complete normalization at 9months. Mild and transient elevation of aminotransferases between 3 and 6months of life were found in 56% and 40% of patient, respectively; non-specific ultrasound cerebral anomalies in absence of clinical neurological signs were found at birth in 9 patients (18%), subsequently normalized. Prenatal maternal screening is of primary importance in order to early detect CCHB, which requires maternal treatment and pacemaker implantation at birth. Infants born to mothers with anti-SSA/Ro Ab should be monitored for all NLS features at birth. However, during the first months of life, these infants seem to develop only mild, transient and self-limited clinical manifestations, which in most cases are completely solved at 9months of life. This consideration, together with the evidence that only 10% of infants had anti-SSA/Ro Ab persistent in blood at 9months, suggests that follow-up of these children can be performed until 6-9months of life with good clinical safety. Moreover, a clinical and laboratory monitoring at 3months of life, when the highest incidence of hematological features and liver tests alterations are observed, is strongly recommended. In the future, it would be clarified if a follow-up until adulthood would be indicated in cases with persistent anti SSA/Ro or in all infants born to mother with anti SSA/Ro.

NGF ligand alters NGF signaling via p75(NTR) and trkA.[Pubmed:10900073]

J Neurosci Res. 2000 Aug 1;61(3):263-72.

Nerve growth factor (NGF) binds to two neurotrophin receptors: p75(NTR) and p140(Trk) (TrkA). Both receptors dimerize in response to NGF binding. TrkA homodimers and heteromers of TrkA and p75(NTR) promote cell survival whereas homodimers of p75(NTR) mediate apoptosis upon binding of NGF. The interaction between receptor and NGF can be inhibited either on the level of the ligand by altering NGF conformation so that NGF is no longer recognized by the receptor or on the level of the receptor by blocking the binding site of p75(NTR) or TrkA. The effect of altering NGF conformation on NGF signaling was investigated in two neuron-like cell lines: in human SK-N-MC cells that express only p75(NTR) and in rat PC12 cells that express both p75(NTR) and TrkA. In the present study we demonstrate that Ro 08-2750 binds to the NGF dimer thereby probably inducing a change in its conformation such that NGF cannot bind to p75(NTR) anymore. In SK-N-MC cells this leads to inhibition of NGF-induced programmed cell death. In PC12 cells enhanced signaling through TrkA was observed.

Description

Ro 08-2750 is a non-peptide and reversible nerve growth factor (NGF) inhibitor which binds to NGF, and with an IC50 of ~ 1 µM. Ro 08-2750 inhibits NGF binding to p75NTR selectively over TRKA. Ro 08-2750 is a selective MSI RNA-binding activity inhibitor, with an IC50 of 2.7 μM.

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