Methotrexate [HRP]

Name: Methotrexate [HRP]
SKU: DAGB319
Rating: 5 (1 reviews)

Methotrexate, HRP-conjugated, Synthetic antigen

COA

SDS

Datasheet

Summary

Specificity

Each conjugate comprises antigen covalently bound to horseradish peroxide and is suitable as a tracer in immunoassay development.

Nature

Synthetic

Tag/Conjugate

HRP

Alternative Names

L-(+)-AMETHOPTERIN; Methotrexate; MTX; ANTIFOLAN; NSC 740; 4-AMINO-N 10-METHYLPTEROYL-L-GLUTAMIC ACID; 4-AMINO-10-METHYLPTEROYLGLUTAMIC ACID; NCI-C04671; (+)-4-AMINO-10-METHYLFOLIC ACID; METHOTREXATE

Format

Liquid

Buffer

Tris-HCl buffer, pH 7.0 with 0.005% Thimerosal and stabilizers

Preservative

None

Storage

Store at 2-8°C for short term. Store at -20°C for long term.

Introduction

Methotrexate is in the class of medications called antimetabolites. The drug is used to treat severe psoriasis, rheumatoid arthritis and certain types of cancer. It works by slowing the proliferation of cells. Specifically, it inhibits the enzyme dihydrofolate reductase that is necessary for the synthesis of folic acid, which is required for the synthesis of DNA, RNA, thymidylates and proteins.

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Documents

pdf COA

pdf SDS

pdf Datasheet

Small Molecule Drug Monitoring

QA & Reviews

Customer Reviews

References

Background Glucocorticoid Therapy Has No Impact on Efficacy and Safety of Abatacept or Adalimumab in Patients with Rheumatoid Arthritis

JOURNAL OF CLINICAL MEDICINE

Authors: Degboe, Yannick; Schiff, Michael; Weinblatt, Michael; Fleischmann, Roy; Ahmad, Harris A.; Constantin, Arnaud

Abstract

To date, the impact of background glucocorticoids (GC) on the efficacy and safety of abatacept or adalimumab in patients with active rheumatoid arthritis (RA) is not clearly established. This post hoc analysis of (AMPLE) trial (NCT00929864) compared efficacy and safety outcomes over 2 years in patients treated with abatacept or adalimumab plus background methotrexate (MTX), who continued GC (<= 10 mg/day) versus those who were not receiving GC (no-GC). Of 646 randomized patients, 317 received abatacept + MTX (161 GC, 156 no-GC) and 326 received adalimumab + MTX (162 GC, 164 no-GC). At Year 2, the adjusted mean changes from baseline in Disease Activity Score (DAS28 C-reactive protein (CRP)) and Health Assessment Questionnaire-Disability Index (HAQ-DI) were not significantly different in the GC versus no-GC subgroups receiving abatacept or adalimumab. A similar proportion of patients achieved remission, HAQ-DI score improvement >= 0.3 and radiographic progression rates. No clinically meaningful safety differences were observed between GC versus no-GC subgroups either with abatacept or adalimumab. In patients with active RA of similar baseline disease activity treated with abatacept or adalimumab plus background MTX, there was no additional value of background GC on clinical, functional or radiographic outcomes over two years.

Chicoric acid prevents methotrexate hepatotoxicity via attenuation of oxidative stress and inflammation and up-regulation of PPAR gamma and Nrf2/HO-1 signaling

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH

Authors: Hussein, Omnia E.; Hozayen, Walaa G.; Bin-Jumah, May N.; Germoush, Mousa O.; Abd El-Twab, Sanaa M.; Mahmoud, Ayman M.

Abstract

Chicoric acid (CA) is a natural antioxidant with promising hepatoprotective activity. We investigated the potential of CA to prevent methotrexate (MTX) hepatotoxicity, pointing to the role of Nrf2/HO-1 signaling and PPAR gamma. Rats received CA for 15 days and were then injected with MTX at day 16. Blood and tissue samples were collected for analysis at day 19. CA ameliorated liver function markers and mitigated histological alterations in MTX-induced rats. Pre-treatment with CA suppressed reactive oxygen species and lipid peroxidation and enhanced antioxidants in MTX-induced rats. Moreover, CA upregulated hepatic Nrf2, HO-1, NQO-1, and PPAR gamma, and attenuated inflammation. Consequently, CA inhibited apoptosis by increasing Bcl-2 expression and suppressing Bax, cytochrome c, and caspase-3 in MTX-administered rats. In conclusion, CA prevented oxidative stress, inflammation, and liver injury induced by MTX by activating Nrf2 /HO-1 signaling and PPAR gamma.