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VX-150 Sale

(Synonyms: N-[1,2-二氢-2-氧代-1-[(膦酰氧基)甲基]-4-吡啶基]-2-(4-氟-2-甲基苯氧基)-4-(三氟甲基)苯甲酰胺) 目录号 : GC63259

VX-150 (EOS-62073) is an orally bioavailable pro-drug that rapidly converts into its active moiety, which is a highly selective inhibitor of NaV1.8 relative to the other sodium channel subtypes (>400-fold).

VX-150 Chemical Structure

Cas No.:1793080-72-4

规格 价格 库存 购买数量
5 mg
¥2,205.00
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10 mg
¥3,510.00
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25 mg
¥7,020.00
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50 mg
¥10,530.00
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产品描述

VX-150 (EOS-62073) is an orally bioavailable pro-drug that rapidly converts into its active moiety, which is a highly selective inhibitor of NaV1.8 relative to the other sodium channel subtypes (>400-fold).

[1] Hemme J Hijma, et, al. Pain Med. 2021 Aug 6;22(8):1814-1826.

Chemical Properties

Cas No. 1793080-72-4 SDF
别名 N-[1,2-二氢-2-氧代-1-[(膦酰氧基)甲基]-4-吡啶基]-2-(4-氟-2-甲基苯氧基)-4-(三氟甲基)苯甲酰胺
分子式 C21H17F4N2O7P 分子量 516.34
溶解度 DMSO : 125 mg/mL (242.09 mM; Need ultrasonic) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 1.9367 mL 9.6835 mL 19.3671 mL
5 mM 0.3873 mL 1.9367 mL 3.8734 mL
10 mM 0.1937 mL 0.9684 mL 1.9367 mL
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Research Update

A Phase 1, Randomized, Double-Blind, Placebo-Controlled, Crossover Study to Evaluate the Pharmacodynamic Effects of VX-150, a Highly Selective NaV1.8 Inhibitor, in Healthy Male Adults

Pain Med 2021 Aug 6;22(8):1814-1826.PMID:33543763DOI:10.1093/pm/pnab032.

Objective: To evaluate the analgesic potential, safety, tolerability, and pharmacokinetics of VX-150, a pro-drug of a highly selective NaV1.8 inhibitor, in healthy subjects. Design: This was a randomized, double-blind, placebo-controlled, crossover study in healthy subjects. Subjects: Twenty healthy male subjects with an age of 18-55 years, inclusive, were enrolled. Eligibility was based on general fitness, absence of current or previous medical conditions that could compromise subject safety, and a training assessment of pain tolerance across pain tests to exclude highly tolerant individuals whose tolerance could compromise the ability to detect analgesic responses. All dosed subjects completed the study. Methods: Subjects were randomized 1:1 to one of two sequences receiving a single VX-150 dose and subsequently placebo, or vice versa, with at least 7 days between dosing. A battery of pain tests (pressure, electrical stair, [capsaicin-induced] heat, and cold pressor) was administered before dosing and repetitively up to 10 h after dosing, with blood sampling up to 24 h after dosing. Safety was monitored throughout the study. Data were analyzed with a repeated-measures mixed-effects model. Results: VX-150 induced analgesia in a variety of evoked pain tests, without affecting subject safety. Significant effects were reported for the cold pressor and heat pain thresholds. Maximum median concentration for the active moiety was 4.30 µg/mL at 4 h after dosing. Conclusion: Results of this proof-of-mechanism study are supportive of the potential of VX-150, a highly selective NaV1.8 channel inhibitor, to treat various pain indications.

Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets

Front Pain Res (Lausanne) 2021 Dec 13;2:750583.PMID:35295464DOI:10.3389/fpain.2021.750583.

The persistence of increased excitability and spontaneous activity in injured peripheral neurons is imperative for the development and persistence of many forms of neuropathic pain. This aberrant activity involves increased activity and/or expression of voltage-gated Na+ and Ca2+ channels and hyperpolarization activated cyclic nucleotide gated (HCN) channels as well as decreased function of K+ channels. Because they display limited central side effects, peripherally restricted Na+ and Ca2+ channel blockers and K+ channel activators offer potential therapeutic approaches to pain management. This review outlines the current status and future therapeutic promise of peripherally acting channel modulators. Selective blockers of Nav1.3, Nav1.7, Nav1.8, Cav3.2, and HCN2 and activators of Kv7.2 abrogate signs of neuropathic pain in animal models. Unfortunately, their performance in the clinic has been disappointing; some substances fail to meet therapeutic end points whereas others produce dose-limiting side effects. Despite this, peripheral voltage-gated cation channels retain their promise as therapeutic targets. The way forward may include (i) further structural refinement of K+ channel activators such as retigabine and ASP0819 to improve selectivity and limit toxicity; use or modification of Na+ channel blockers such as vixotrigine, PF-05089771, A803467, PF-01247324, VX-150 or arachnid toxins such as Tap1a; the use of Ca2+ channel blockers such as TTA-P2, TTA-A2, Z 944, ACT709478, and CNCB-2; (ii) improving methods for assessing "pain" as opposed to nociception in rodent models; (iii) recognizing sex differences in pain etiology; (iv) tailoring of therapeutic approaches to meet the symptoms and etiology of pain in individual patients via quantitative sensory testing and other personalized medicine approaches; (v) targeting genetic and biochemical mechanisms controlling channel expression using anti-NGF antibodies such as tanezumab or re-purposed drugs such as vorinostat, a histone methyltransferase inhibitor used in the management of T-cell lymphoma, or cercosporamide a MNK 1/2 inhibitor used in treatment of rheumatoid arthritis; (vi) combination therapy using drugs that are selective for different channel types or regulatory processes; (vii) directing preclinical validation work toward the use of human or human-derived tissue samples; and (viii) application of molecular biological approaches such as clustered regularly interspaced short palindromic repeats (CRISPR) technology.