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minocycline hydrochloride

✓ Approved

PreCision Dermatology · 小分子 · 小分子

什么是 minocycline hydrochloride？

minocycline hydrochloride 是一种小分子，由PreCision Dermatology研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

公司PreCision Dermatology
药物类别小分子
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, PreCision Dermatology

治疗适应症

minocycline hydrochloride 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsStreptococcal infection✓ Approved

相关研究文献

PubMedOrganic letters2026-07-27

Divergent Access to Chiral Pyrrolidinone-Fused 4H-Pyrans and Pyridines Via Organocatalytic Asymmetric Decarboxylative Addition-Annulation of β-Keto Acids with 2,3-Dioxopyrrolidines.

Li Tianxing T, He Tianyu T, Meng Weiyue W, Jin Hui H et al.

We disclose an unprecedented organocatalytic asymmetric decarboxylative Michael addition of β-keto acids to 2,3-dioxopyrrolidines, enabling the efficient assembly of chiral pyrrolidinone-fused [3,4-b]-4H-pyrans and [3,4-b]-pyridines. The reaction affords chiral pyrrolidinone-tethered 1,5-dicarbonyl intermediates in high yields with excellent regio- and enantioselectivities. Acid-promoted intramolecular cyclization of these adducts provides enantioenriched pyrrolidinone-fused [3,4-b]-4H-pyrans without erosion of enantiopurity, whereas cyclocondensation with hydroxylamine hydrochloride delivers diverse pyrrolidinone-fused [3,4-b]-pyridines. Notably, this protocol is compatible with a one-pot tandem process and gram-scale synthesis.

PMID 42504541
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PubMedToxins2026-07-27

Enhanced Protection Against Toxicity of Nemopilema nomurai Venom Using a PEG-EGCG/Tetracycline Hydrochloride Micellar Nanocomplex.

Li Jie J, Hu Yanan Y, Qian Yunfeng Y, Luo Sai S et al.

Jellyfish stings are the most common type of marine life injuries. However, at present, the treatment measures against jellyfish stings are mostly empirical and supportive, with uncertain therapeutic outcomes, and there is a lack of specific antidotes based on the toxic mechanism of jellyfish venom in clinical practice. In our previous study, polyphenol epigallocatechin-3-gallate (EGCG) was found to neutralize the toxicity of jellyfish Nemopilema nomurai venom (NnV) in vivo and in vitro. Herein we further demonstrated that EGCG exerted its antagonistic effect against NnV through inhibiting the oxidative stress, pro-apoptotic proteins, and systemic inflammatory responses. Subsequently, we constructed a polyethylene glycol (PEG)-EGCG/tetracycline hydrochloride (HTC) co-loaded micellar nanocomplex in order to enhance the stability and bioavailability of EGCG in vivo, which successfully integrated the membrane-repair function of PEG, the enzyme inhibitory effect of HTC and the antioxidant properties of EGCG. Notably, this micellar nanocomplex demonstrated significant protective effects against both functional damage and pathological alterations in a non-lethal NnV-envenomed mouse model. When administered 1 h after NnV envenomation, EGCG (40 mg/kg), HTC and PEG-EGCG (containing 40 mg/kg EGCG) only partially improved abnormal blood biochemical indicators and moderately alleviated histopathologic damage, and PEG-EGCG/HTC containing merely 8 mg/kg EGCG completely mitigated the toxic reactions in envenomed mice. In the preventive regimen, the administration of EGCG, HTC or PEG-EGCG 30 min before exposure showed no significant improvement in abnormal blood biochemical indicators and histopathologic damage, while PEG-EGCG/HTC could still significantly improve the functional impairments and histopathologic damage of the heart and liver in NnV-envenomed mice. These findings suggest the clinical translational potential of PEG-EGCG/HTC against jellyfish envenomation.

PMID 42506698
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PubMedAnalytical methods : advancing methods and applications2026-07-27

Smartphone-based fluorescence sensing platform for tetracycline determination based on a high quantum yield europium metal-organic framework with a dual-ligand strategy.

Cheng Shuang S, Song Jintian J, Wen Yue Y, Xu Yijia Y et al.

Ultrasensitive and visual detection of tetracyclines (TCs) is of great significance to public health and environmental safety. Herein, we synthesized a dual-ligand europium metal-organic framework (Eu-phen-MOF) via a one-step solvothermal method for the fluorescence detection of TCs. Compared with the Eu-MOF without 1,10-phenanthroline, Eu-phen-MOF exhibits superior stability, lower LOD and higher quantum yield. It delivers superior TC sensing performance and anti-interference, enabling high-accuracy detection with limits of 152.0 nmol L-1, 249.4 nmol L-1, 171.0 nmol L-1 and 277.7 nmol L-1 for tetracycline (TC), oxytetracycline (OTC), doxycycline hydrochloride (DOX), and chlortetracycline (CTC), respectively. Eu-phen-MOF was used for the quantitative detection of TC, OTC, DOX, and CTC in real samples (milk, eggs, and river water) and recoveries ranging from 94.64% to 105.37% were achieved. Finally, a portable fluorescence sensing platform integrating a smartphone and the Eu-phen-MOF fluorescent hydrogel was constructed, enabling convenient, rapid, and low-cost detection of TCs. This work not only highlights the significance of the dual-ligand strategy for fabricating an efficient TC sensor, but also develops a rapid and visual method for TC detection.

PMID 42504902
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PubMedMicrobiology spectrum2026-07-27

Mocravimod as a repurposing drug against clinical isolates of Staphylococcus aureus by targeting cell membrane.

Tang Yuanyuan Y, Xia Yuqing Y, Huang Xuancheng X, Yu Zhijian Z et al.

Staphylococcus aureus infections, particularly those caused by multidrug-resistant strains and associated with biofilm formation, pose a major therapeutic challenge in clinical practice. The objective of this study was to evaluate the antibacterial and antibiofilm activity of mocravimod (KRP-203), an FDA-approved S1P receptor modulator, against clinical S. aureus isolates and to explore its underlying mechanism of action. The antibacterial activity of KRP-203 was assessed against methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) using MIC determination, time-kill assays, and biofilm inhibition models. KRP-203 exhibited strong bactericidal activity against planktonic MSSA and MRSA, with MIC values ranging 6.25-50μM. Time-kill assays demonstrated rapid bacterial eradication at 8× MIC within 2 h, showing superior killing kinetics compared with vancomycin. At sub-inhibitory concentrations, KRP-203 inhibited biofilm formation by up to 70% and reduced viable bacterial counts in mature biofilms by >2.5 logs. To elucidate the antibacterial mechanism, whole-genome sequencing and quantitative proteomic analyses were performed. These analyses revealed mutations in membrane-associated genes, including glnQ and BCAT, and significant alterations in proteins related to membrane integrity and redox regulation. Consistently, functional assays confirmed that KRP-203 disrupts bacterial cell membrane, as evidenced by dose-dependent membrane depolarization, increased permeability, and direct binding to cardiolipin and phosphatidylglycerol. Molecular docking further predicted a favorable interaction between KRP-203 and GlnQ. In conclusion, KRP-203 demonstrated notable antibacterial and antibiofilm activity against S. aureus, likely through membrane integrity disruption. While these findings highlight its potential as a repurposed antibacterial agent, further studies are required to fully elucidate its molecular targets, optimize antibacterial efficacy, and evaluate its in vivo safety profile. Antibiotic resistance and the formation of biofilms, which protect bacteria from medications and immunological responses, present the significant challenges for the clinical treatment of Staphylococcus aureus infections. This study reveals mocravimod hydrochloride (KRP-203), a clinically approved drug initially intended to treat leukemia, as a viable new candidate against S. aureus infection. KRP-203 quickly kills both drug-susceptible and resistant S. aureus, including difficult-to-treat biofilm-associated cells. Its membrane-disrupting activity quickly kills drug-resistant bacteria while also destroying biofilm formations, presenting a dual action rarely accomplished by conventional antibiotics. Critically, KRP-203's established safety profile in human studies may hasten its repurposing as a new weapon against biofilm-associated infections, providing possible solutions for chronic and drug-resistant S. aureus infections where existing treatments commonly fail.

PMID 42505145
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PubMedJournal of pharmaceutical sciences2026-07-26

Formulation development and evaluation of nasal in situ gel of promethazine hydrochloride- part II: Pharmacokinetic evaluation and bioavailability studies.

Patil Surabhi H SH, Patil Sanjay B SB

Promethazine hydrochloride, a first-generation H1 receptor blocking agent, possesses antimuscarinic, sedative, and serotonin antagonistic properties. It is widely used as an antiemetic for treating nausea and vomiting caused by motion sickness, vertigo, postoperative and drug-induced vomiting, and Meniere's disease. Although extensively absorbed after oral administration, it undergoes significant first-pass metabolism, resulting in poor bioavailability of about 25 %. To overcome this limitation and improve patient compliance, the nasal route was explored owing to its high vascularity, large surface area, and absence of first-pass metabolism. The major drawback of nasal delivery, mucociliary clearance (MCC), was addressed by formulating a thermosensitive mucoadhesive in situ hydrogel, enhancing residence time and bioavailability. The study aimed to evaluate the safety, stability, and bioavailability of the intranasal in situ hydrogel of promethazine hydrochloride. Safety was assessed using freshly excised sheep nasal mucosa, while accelerated stability studies confirmed formulation stability. In vivo studies were performed using New Zealand White rabbits, and pharmacokinetic parameters were calculated by the trapezoidal rule using a validated HPLC method. The optimized formulation exhibited a Cmax of 296.18 ng/ml, Tmax of 1 hour, and bioavailability of 36.42 %, which is 62.58 % higher than after oral administration, indicating intranasal in situ hydrogel as a promising approach for enhancing bioavailability of antiemetic drugs.

PMID 42501944
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PubMedTranslational neuroscience2026-07-26

The activation of glial cells in the medulla visceral zone impairs synaptic plasticity and promotes inflammation and immune disorders in sepsis.

Wang Jianjian J, Wang Lizhi L, Jiang Weiwei W, Zhu Lu L et al.

Sepsis elicits neuroinflammation in the medullary visceral zone (MVZ), which disrupts the cholinergic anti-inflammatory pathway (CAP). However, the underlying mechanisms and translational therapeutic potential remain poorly defined. Adult male Sprague-Dawley rats received either intracerebroventricular lipopolysaccharide (LPS; 25 μg/25 μL) to induce MVZ neuroinflammation model rats, or intraperitoneal LPS (6 mg/kg) to establish polymicrobial sepsis model rats. Anti-inflammation groups were involved with minocycline sucrose solution (120 mg/L) which was administered by drinking for 4 days prior to LPS challenge. CAP transection groups were undergone right cervical vagotomy 7 days before anti-inflammation interventions. Murine sepsis score (MSS), mortality rates, heart rate variability (HRV), cytokine levels in blood and medulla, systemic immunity level, and the expression levels of glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (IBA-1), CD22, tumor necrosis factor-α (TNF-α), Munc13-1, Synaptophysin (SYN), and postsynaptic density protein 95 (PSD-95) in the MVZ were measured and analyzed. Both sepsis and MVZ neuroinflammation model rats showed significantly increased mortality and MSS scores, depressed HRV parameters, and upregulated expressions of GFAP, IBA-1, CD22, and TNF-α, with downregulated expressions of Munc13-1, SYN, and PSD-95 in the MVZ. Synaptic structural damage including reduced synaptic vesicles, decreased RT1.D expression on lymphocytes, increased percentages of Th17 and Treg lymphocytes, and increased serum levels of TNF-α, IL-10, and INF-γ were observed. Anti-inflammatory intervention reversed these changes in both model rats, whereas CAP transection partially abolished the anti-inflammatory benefits, confirming CAP dependence. Sepsis-induced MVZ neuroinflammation dismantles synaptic integrity and CAP modulation, which intensifies peripheral cytokine storm. Early central anti-inflammation repairs MVZ synaptic plasticity and reinstates vagal immunomodulation, which may provide a translational strategy to limit septic escalation.

PMID 42502433
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