Delving into the Latest Updates on Hydrocodone bitartrate with Synapse

Overview

Basic Info

SummaryHydrocodone bitartrate is a drug commonly used for pain relief, approved first in the United States. The drug works by binding to opioid receptors in the brain, acting as a mu/kappa/delta agonist. Its chemical name is 4,5(alpha)-epoxy-3-methoxy-17-methylmorphinan-6-one tartrate (1:1) hydrate (2:5) or morphinan-6-one, 4,5-epoxy-3-methoxy-17-methyl-, (5 alpha)-, [R (R*, R*)]-2,3-dihydroxybutanedioate (1:1),hydrate (2:5). Hydrocodone bitartrate is widely used in the U.S. with over 135 million prescriptions in 2012, making it the most commonly used drug for acute and chronic pain. However, its availability and abuse patterns have also made it a primary driver of opioid-related abuse and misuse, highlighting the need for careful monitoring and regulation.

Drug Type

Small molecule drug

Synonyms

酒石酸氢可酮, AFI-001, ATLP-03

+ [9]

Target

Opioid receptors

Action

agonists

Mechanism

Opioid receptors agonists(Opioid receptors agonists)

Therapeutic Areas

Nervous System DiseasesOther Diseases

Active Indication

Pain

Inactive Indication

Chronic osteoarthritisChronic PainLow Back Pain+ [2]

Originator Organization-

Active Organization

Purdue Pharma LP

Knoa Pharma LLC

Inactive Organization

Teva Branded Pharmaceutical Products R&D LLC

Zogenix, Inc.

Societal CDMO Gainesville LLC

+ [1]

License Organization-

Drug Highest PhaseApproved

First Approval Date

United States (25 Oct 2013),

Pain

Regulation-

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Structure/Sequence

Molecular FormulaC22H29NO10

InChIKeyZICRJLQTAUVSDU-NSJZFRMTSA-N

CAS Registry34195-34-1

High-yielding dairy cows around parturition are challenged by varying degrees of low calcium status (hypocalcemia), which is associated with increased risk of several metabolic disorders and diseases in early lactation. The aim of the present study was to investigate effects of dietary 25-hydroxycholecalciferol (25-OH-D₃; calcidiol) supplementation during the transition period. Forty-two multiparous Holstein cows were fed 1 of 2 treatments: either cholecalciferol (D₃) or 25-OH-D₃ (HyD) as dietary vitamin D supplements. From 21 d before the expected calving until parturition, the D₃ group received 0.475 mg/d (0.035 mg/kg of DM) of D₃, and the HyD group received 1.45 mg/d (0.108 mg/kg of DM) of 25-OH-D₃. From parturition until 21 DIM, the D₃ group received 0.625 mg/d (0.024 mg/kg of DM) of D₃, and the HyD group received 0.625 mg/d (0.024 mg/kg of DM) of D₃ plus 1.0 mg/d of 25-OH-D₃ (0.056 mg/kg of DM). Arterial blood samples were collected by puncture of a. auricularis on d -21, -7, -3, 0 (calving day), and +1 relative to calving for analysis of blood ionized Ca. Blood samples were taken from the tail on d -21 (22 ± 5 d), -7 (6 ± 2 d), -3 (2 ± 1 d), 0 (d 0; 13 ± 8 h after calving), 1 (36 ± 11 h after calving), 10 (9 ± 2 d), and 20 (16 ± 2) relative to calving to analyze plasma 25-OH-D₃ level, plasma minerals, and other plasma metabolites. During the entire experiment, cows were fed TMR, and DMI, productive performance, metabolic disorders, and other diseases were recorded. Milk yield, milk protein percentage, milk lactose percentage, BCS, and BW were not affected by treatment. There was an interaction between treatment and time for DMI. The DMI in HyD was numerically lower compared with D₃ at d -3, -2, and -1 relative to calving; however, the DMI in HyD was numerically higher compared with D₃ at d 0, 1, and 2 postpartum. Plasma 25-OH-D₃ was higher in HyD compared with D₃ both pre- and postpartum; however, plasma 1,25(OH)₂D₃ was not affected by treatment. Arterial blood ionized Ca was affected by treatment, and it was higher in the HyD (1.08 ± 0.02) compared with the D₃ on the day of calving (0.99 ± 0.02 mmoL/L; lsmeans ± SEM). There was a tendency for lower incidence of mastitis in HyD compared with D₃. Plasma BHB level (lsmeans ± SEM) was significantly lower in HyD (0.61 ± 0.02) compared with D₃ (0.70 ± 0.02 mM). In conclusion, feeding 25-OH-D₃ to transition dairy cows increased arterial blood ionized Ca on the day of calving compared with cows supplemented with D₃. The increased arterial blood ionized Ca in HyD was apparently mediated by 25-OH-D₃ without affecting plasma 1,25-(OH)₂D₃. Additionally, the results showed a lower incidence of mastitis in HyD.

01 Jun 2026·AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY

Fluid restriction enhances mitochondrial stress in peripheral blood mononuclear cells following high-volume resistance exercise in health young males

Article

Author: Sekiguchi, Yasuki ; Appell, Casey R. ; Jiwan, Nigel C. ; Levitt, Danielle E. ; Vellers, Heather L. ; Luk, Hui-Ying

This study examined how 24-h fluid restriction affects mitochondrial stress and inflammatory responses in peripheral blood mononuclear cells (PBMCs) after high-volume resistance exercise in young men. Dehydration increased markers of mitophagy (PINK1 and p-DRP1 S616 ), autophagosome formation (LC3-II and p62), and oxidative stress (H 2 O 2 ), while systemic IL-6 and CRP were elevated compared with euhydration. Findings suggest dehydration amplifies mitochondrial stress and proinflammatory signaling, highlighting the importance of proper hydration during exercise and its implications on cellular homeostasis.

01 Jun 2026·BIOMEDICAL CHROMATOGRAPHY

Haizao Yuhu Decoction Inhibits Goiter via p53 Pathway‐Induced Apoptosis: Metabolomic and Cellular Assay Analysis

Article

Author: Liu, Xiaoqing ; Wu, Yinghao ; Zhang, Shujing ; Zhong, Gansheng ; Xu, Xiangnan ; Chen, Shaohong ; Liao, Wenyong ; Wu, Meijing ; Liu, Haiyan ; Xiu, Linlin ; Zhang, Jiwen

ABSTRACT:

Haizao Yuhu Decoction (HYD), a classic Traditional Chinese Medicine (TCM) formula, is used to treat Yingbing, which corresponds to goiter in modern medicine. Although HYD has been extensively studied for goiter, its specific active components and the underlying mechanisms of action remain to be fully elucidated. This study investigated the effects and mechanisms of HYD in goiter using untargeted LC–MS metabolomics (comparing HYD decoction and HYD‐containing serum), network pharmacology for target prediction, and in vitro validation with a TSHR human monoclonal antibody M22 (TSHR hMAb M22)‐induced thyroid cell proliferation model, followed by Western blotting to verify key pathway proteins. The comparison of metabolomic profiles between HYD decoction and HYD‐containing serum revealed that 2091 metabolites (90.05%) were downregulated, while 231 were upregulated in medicated serum. Network pharmacology predicted targets including AKT1, PIK3CA, ESR2, ESR1, and TP53. HYD‐containing serum exhibited pro‐apoptotic effects on the cell proliferation model. The underlying mechanism may primarily involve the upregulation of the p53/PUMA/p21 pathway, which subsequently affects caspase‐3 activity. Furthermore, the action of HYD may involve non‐p53 multiple signaling pathways. HYD may exert its effects by modulating multiple signaling pathways, including p53/PUMA/p21, leading to apoptosis in thyroid cells.

53

News (Medical) associated with Hydrocodone bitartrate

12 May 2026

·www.biospace.com

DIMERx Preclinical Data Confirms DMX-101 Non-Addictive Profile: No Reinforcement, No Dependence

Key Regulatory Benchmark Met, Differentiating DMX-101 from Traditional Opioid Analgesics Late-Breaking Results to be Presented at CPDD 2026 Annual Meeting San Francisco, California--(News - May 12, 2026) - DIMERx, Inc. ("DIMERx" or "the Company") is a clinical-stage biopharmaceutical company dedicated to addressing the public-health crisis of drug misuse and dependence, with a portfolio of first-in-class, dimer-based pain therapeutics engineered to deliver effective analgesia without the addiction liabilities of conventional opioids. In June 2025, DIMERx was awarded a NIH HEAL Initiative grant to advance its DMX-101 program. The company today announced preclinical data confirming that DMX-101, an orally bioavailable, peripherally acting new chemical entity (NCE) dimer of buprenorphine, is free of the reinforcing effects that drive addiction to traditional opioids. In a self-administration study conducted in accordance with FDA guidance, cocaine- and hydrocodone-trained rats demonstrated that DMX-101 produced no reinforcing behavior characteristic of opioid misuse and dependence. All compounds were administered intravenously to maximize pharmacological exposure, representing a worst-case scenario for misuse potential assessment. Notably, DMX-101 plasma exposure levels in rats were 18-fold higher than the maximum plasma concentration (Cmax) observed in humans following oral dosing, indicating that the absence of rewarding effects was demonstrated at exposures substantially exceeding those expected in clinical use. Even under these rigorous conditions, DMX-101 showed no evidence of addictive behavior, supporting a favorable safety pro respect to misuse liability, overdose risk, and opioid-related morbidity. "DMX-101 is designed to exclusively target peripheral opioid receptors, blocking pain signals at their source without engaging central nervous system pathways linked to reward, sedation, or addiction, and the absence of self-administration behavior observed in this study supports the potential for DMX-101 to provide effective pain relief without the risk of misuse," said Virginia Sanders, PhD, Vice President of Preclinical and Principal Investigator for the NIH grant. "These results, together with prior preclinical and clinical findings, confirm our core hypothesis that peripherally restricted opioid modulation can deliver meaningful analgesia without the liabilities of traditional opioids. As the clinical and societal need for safer pain therapies intensifies, DMX-101 represents a differentiated approach to delivering meaningful analgesia without cognitive impairment or contributing to the addiction epidemic." "DMX-101 could redefine pain treatment. The absence of rewarding effects, even at exposures 18-fold above clinical levels, suggests we are looking at a genuinely differentiated therapy, one with the potential to displace traditional opioids and change the trajectory of the addiction crisis," said Eric C. Strain, MD, Professor of Psychiatry and Behavioral Sciences at Johns Hopkins University School of Medicine and an expert in addiction medicine and Scientific Advisor to DIMERx. DIMERx will present these findings at the College on Problems of Drug Dependence (CPDD) 88th Annual Meeting, June 13-17, in Portland, OR. Virginia Sanders, PhD and Eric C. Strain, MD, will present the data. Poster Details: Title: DMX-101 Does Not Exhibit Reinforcing Effects in a Hydrocodone-Trained Rat Self-Administration Model Session: Poster II Date/Time: Monday, June 15, 2026; 5:00pm-6:30pm Location: OCC, Level 1, Exhibit Hall A About DIMERx, Inc. DIMERx, Inc. is a clinical-stage biopharmaceutical company developing first-in-class, covalently linked dimer-based therapeutics to address major public-health challenges in pain management and the opioid crisis. Co-founded by CEO Nikhilesh Singh, M.Pharm, PhD, and CFO/COO Gregory Beyer, DIMERx is building a pipeline of innovative dimer-based candidates targeting pain and other serious conditions with high unmet medical need. The company's lead asset, DMX-101, is a covalently modified, chemically stable, halogen-free buprenorphine dimer (CAS No: 1820753-68-1) that acts peripherally at the source to provide non-addictive pain relief. DMX-101 is in phase 2 clinical development for chronic lower back pain. Across Phase 1 and Phase 2a studies involving over 400 subjects and patients, it has demonstrated a favorable safety profile, including pancreatic safety, and clear analgesic benefits. The DMX-101 program, which includes a planned human abuse liability study, is supported by a grant awarded by the National Institute on Drug Abuse (NIDA) under the NIH HEAL Initiative. DIMERx's second program, DMX-201, is a covalently linked dimer of arginine and agmatine, a next-generation nitric oxide (NO) donor being developed for conditions involving endothelial dysfunction, such as vaso-occlusive crisis (VOC) pain in sickle cell disease, where treatment options remain dominated by centrally acting opioids. Learn more at . Funding Disclosure and Forward-Looking Statements Research reported in this press release was supported by the National Institute on Drug Abuse of the National Institutes of Health under award number 1 UG3 DA061645-01A1. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. This press release may contain forward-looking statements, including information about management's view of DIMERx ("the Company"), future expectations, plans and prospects. In particular, when used in the preceding discussion, the words "believes," "expects," "intends," "plans," "anticipates," or "may," and similar conditional expressions are intended to identify forward-looking statements. Any statements made in this presentation other than those of historical fact, about an action, event or development, are forward-looking statements. These statements involve known and unknown risks, uncertainties and other factors, which may cause the results of the Company, its subsidiaries and concepts to be materially different than those expressed or implied in such statements. Unknown or unpredictable factors also could have material adverse effects on the Company's future results. The forward-looking statements included in this presentation are made only as of the date hereof. The Company cannot guarantee future results, levels of activity, performance or achievements. Accordingly, you should not place undue reliance on these forward-looking statements. Finally, the Company undertakes no obligation to update these statements after the date of this release, except as required by law, and also takes no obligation to update or correct information prepared by third parties that are not paid for by DIMERx. Investor Contact Hanover International Inc. Kathy Cusumano, President IR@dimerx.com To view the source version of this press release, please visit

Phase 2Clinical Result

28 Jan 2026

·www.prnewswire.com

Elysium Therapeutics Raises $7.5 Million SAFE Round to Accelerate Development of Novel Rescue Therapy Designed to Specifically Combat Oral Fentanyl Overdose

LYONS, Colo., Jan. 28, 2026 /PRNewswire/ -- Elysium Therapeutics, an emerging biopharmaceutical company developing treatments specifically designed to prevent and reverse overdoses caused by highly potent, synthetic opioids especially when ingested orally, today announced that it has completed a $7.5 million SAFE round. Elysium intends to accelerate development of its SOOPR™ (Synthetic Opioid Overdose Protection and Reversal) technology designed specifically as a rescue treatment for overdoses brought on by synthetic opioids, including fentanyl and the emerging threat of more potent nitazenes. "With these funds in place, we have initiated work to progress our SOOPR technology through preclinical and clinical studies as we develop this important, life-saving technology to address the deadly overdose epidemic caused by illicit synthetic opioids," said Greg Sturmer, CEO of Elysium Therapeutics. "Our society continues to see far too many overdose fatalities, and we believe that our SOOPR technology has enormous potential to become the new standard for rescue and as a countermeasure as the illicit drug market evolves to progressively more dangerous opioids." SOOPR is a rapid-onset, long-acting rescue agent specifically designed to prevent and reverse overdoses from synthetic opioids, including oral fentanyl and nitazenes. SOOPR utilizes a proprietary naloxone prodrug formulation that offers more rapid onset and longer duration of action than current rescue agents (e.g., NARCAN, Kloxxado, Opvee). The technology is designed to rapidly restore respiration, reducing the risk of hypoxic brain injury and death, and provide 12 – 24 hours of effective opioid blockade to minimize the risk of re-narcotization. Further, SOOPR delivers naloxone with a unique, infusion-like pharmacokinetic profile that is ideally suited to reduce the risk of severe withdrawal symptoms commonly associated with nalmefene and high-dose naloxone products. SOOPR is also intended to prevent same-day re-use of opioids and to offer an essential period for family members and healthcare professionals to assist the overdose patient in accessing medically-assisted therapy, which represents their best opportunity for long-term survival. Data from in vivo proof-of-concept studies of SOOPR demonstrated a more rapid onset of action versus intranasal and intramuscular naloxone and a significantly longer duration of action. This profile is specifically designed to counteract oral fentanyl and nitazene overdoses associated with prolonged exposures that often outlast the short-acting profile of existing rescue agents. About Elysium Therapeutics Elysium is an emerging biopharmaceutical company developing treatments specifically designed to rescue and reverse overdoses caused by oral synthetic opioids, including fentanyl and nitazenes. Elysium is working to establish new standards of safety in the opioid industry by developing SMART™ (Safer Medicines Alleviate Risks and Trauma) products, first- and best-in-class medicines that address the limitations and dangers associated with opioids and overdose rescue agents to reduce suffering from opioid-use disorder, opioid overdose, and acute pain. Elysium's lead technology, SOOPR™ (Synthetic Opioid Overdose Prevention and Reversal), is a fast-onset, long-acting opioid antagonist specifically designed to address oral synthetic opioid overdose. Tens of thousands of unnecessary overdose deaths each year exemplifies the critical shortcomings of currently available rescue agents, including NARCAN and Opvee. In addition, Elysium is also developing oral-overdose protected (O2P™) hydrocodone for the treatment of moderate-to-severe acute pain, having achieved human proof-of-concept demonstrating a significant reduction in hydrocodone exposure in overdose scenarios versus generic hydrocodone. For more information, please visit . SOURCE Elysium Therapeutics 21% more press release views with Request a Demo

14 Nov 2025

·www.drugs.com

Nonopioids Superior to Opioids on Day 1 After Third Molar Extraction

FRIDAY, Nov. 14, 2025 -- For patients undergoing impacted mandibular third molar extraction, nonopioid therapy provides superior pain control on day 1 and noninferior control to opioids on days 2 and 3, according to a research letter published online Nov. 6 in JAMA Network Open . Janine Fredericks-Younger, D.M.D., from the Rutgers School of Dental Medicine in Newark, New Jersey, and colleagues conducted a multisite, noninferiority trial to compare the analgesic effectiveness of a nonopioid combination ( ibuprofen 400 mg and acetaminophen 500 mg) with an opioid combination (hydrocodone 5 mg and acetaminophen 300 mg) for postoperative pain management after extraction of an impacted mandibular third molar. Of the 1,815 participants, 909 received a nonopioid combination and 906 received an opioid. The researchers found that on day 1, nonopioids provided superior pain relief for females and males (mean difference, −0.63 and −0.75, respectively). Nonopioids were noninferior on days 2 and 3 and during the postoperative period, with all confidence intervals within the margin of noninferiority. The nonopioid group had higher patient satisfaction, with 82.8 and 87.8 percent of females and males, respectively, reporting being extremely satisfied in the nonopioid group compared with 76.2 and 81.6 percent, respectively, in the opioid group (odds ratios, 1.51 and 2.20 for females and males, respectively). "We feel pretty confident in saying that opioids should not be prescribed routinely for dental procedures," Fredericks-Younger said in a statement. "Our nonopioid combination really should be the analgesic choice." One author disclosed ties to the pharmaceutical industry. Abstract/Full Text

Clinical Result

100 Deals associated with Hydrocodone bitartrate

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External Link

KEGG	Wiki	ATC	Drug Bank
-	Hydrocodone bitartrate	R05DA03	-

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Pain	United States	Societal CDMO Gainesville LLC	25 Oct 2013

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Osteoarthritis	Phase 3	United States	Teva Branded Pharmaceutical Products R&D LLC	01 Nov 2010
Chronic Pain	Phase 3	United States	Zogenix, Inc.	01 May 2010
Low Back Pain	Phase 3	United States	Zogenix, Inc.	01 Mar 2010
Chronic osteoarthritis	Phase 2	-	Zogenix, Inc.	01 Sep 2002
Pain, Postoperative	Phase 2	-	Zogenix, Inc.	01 Aug 2002

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01402375 (CTgov)	Phase 3	Analgesia \| Acute Pain	720	Hydrocodone (first trial) (Hydrocodone (First Trial))	pcqpoonqag(jiudtrgjiq) = iudjkmkaat tqemajkars (bhkdysaqkt, 1.7) View more	-	01 May 2018
				Codeine (Codeine (First Trial))	pcqpoonqag(jiudtrgjiq) = iriotcrovh tqemajkars (bhkdysaqkt, 1.8) View more
NCT01240863 (CTgov)	Phase 3	Low Back Pain \| Osteoarthritis \| Chronic Pain	391	Placebo (Placebo (Double-blind Treatment Period))	xlhzefchji(oibbnxaswg) = juonldhadd cfuffmslar (udtidemnzl, 0.169) View more	-	05 Jun 2017
				Hydrocodone ER (Hydrocodone ER (Double-blind Treatment Period))	xlhzefchji(oibbnxaswg) = guxucqemqq cfuffmslar (udtidemnzl, 0.176) View more
NCT01922739 (CTgov)	Phase 3	Low Back Pain	182	Placebo+Hydrocodone ER	opofxvapbk = yexlbcmoud ugkslhbura (flqumjgqmg, ugpyaultrl - uucfjpwvsu) View more	-	02 Jun 2017
NCT01789970 (CTgov)	Phase 3	Low Back Pain	625	Placebo (Placebo (Double-blind Treatment Period))	rkhvpyiddj(bgtezbridq) = zjgrzftuqi jscpfhgayp (clelxfhaou, 0.145) View more	-	05 Apr 2017
				Hydrocodone ER (Hydrocodone ER (Double-blind Treatment Period))	rkhvpyiddj(bgtezbridq) = oadaplwwcg jscpfhgayp (clelxfhaou, 0.134) View more
NCT01517295 (CTgov)	Phase 4	Chronic Pain	30	Hydrocodone (Group 1)	uzzdmvogtb(yuocyveqal) = tfcloruans gmtepjdhlh (dtzchmmxge, 0) View more	-	28 Jul 2016
				Hydrocodone (Group 2)	uzzdmvogtb(yuocyveqal) = ochrnyuhhh gmtepjdhlh (dtzchmmxge, 0) View more
NCT01859715 (CTgov)	Not Applicable	Medication interactions	502	Oxycodone (Oxycodone Group)	gsaewpehfu(exlcyxxbad) = mhiwiztojh vymdleaahk (khixlglqma, vammsvcmvq - pnaxfsujjx) View more	-	05 May 2016
				Hydrocodone (Hydrocodone/Acetaminophen Group)	gsaewpehfu(exlcyxxbad) = hglqvvgkqy vymdleaahk (khixlglqma, qqdwizegpf - gttdfeqhvz) View more
NCT01452529 (CTgov)	Phase 3	Low Back Pain	905	Hydrocodone bitartrate (Hydrocodone Bitartrate)	fydlwzhvwh(twyrbbpvkj) = wnpftdmrkl rispuajzrw (hlxcdkyfxv, 0.13) View more	-	04 Dec 2014
				Placebo to match hydrocodone bitartrate q24h tablets (Placebo)	fydlwzhvwh(twyrbbpvkj) = lgeqpdbqzg rispuajzrw (hlxcdkyfxv, 0.13) View more
NCT01400139 (CTgov)	Phase 3	Chronic Pain	922	Hydrocodone bitartrate (HYD) (HYD Core Study)	uibqgtaons = svtmdsuvef yuvootxjwl (dxckcumsut, dcbnanclef - tmacmowwom) View more	-	04 Dec 2014
				Hydrocodone bitartrate (HYD) (HYD Extension Period)	uibqgtaons = eeekguerzk yuvootxjwl (dxckcumsut, xbwatteapi - giierevojt) View more
NCT01115569 (CTgov)	Phase 3	Chronic Pain	424	Hydrocodone Bitartrate (Open-label Hydrocodone Bitartrate Extended Release Capsules)	rnczvelkym(dmltnlgkto) = vcxpgxmzkh kkfqheyohw (yleaffpqez, 2.2)	-	25 Apr 2014
				Hydrocodone Bitartrate (Conversion/Titration Phase)	yvtcfgmddd(jicdhjpvhm) = eusmxizzoy qkmmvsyzqo (yzhyxdgfev, hxblnrpuqn - cpkyclljft) View more
NCT01081912 (CTgov)	Phase 3	Low Back Pain	510	Hydrocodone bitartrate (Hydrocodone Bitartrate Capsules)	dmtnlxhpxs(hzgcsuqvez) = xdsfobpdjw elsdyxsrqn (luafannuvg, 1.563)	-	21 Apr 2014
				Placebo (Placebo Comparator)	dmtnlxhpxs(hzgcsuqvez) = ywdbjrqrxx elsdyxsrqn (luafannuvg, 1.550)