#NMDA receptor antagonist

[dynamichealthinsights]

Unraveling the Tapestry of Alzheimer's Medications: A Deep Dive into Treatment Options

Alzheimer’s disease, often described as a thief of memories, is a relentless neurodegenerative disorder that gradually erodes cognitive abilities, impacting not only the individual but also their loved ones. While the quest for a cure continues, medications play a vital role in managing symptoms, slowing progression, and enhancing the quality of life for those navigating this challenging journey.…

[transgenderer]

The real or perceived proximity to death often results in a non-ordinary state of consciousness characterized by phenomenological features such as the perception of leaving the body boundaries, feelings of peace, bliss and timelessness, life review, the sensation of traveling through a tunnel and an irreversible threshold. Near-death experiences (NDEs) are comparable among individuals of different cultures, suggesting an underlying neurobiological mechanism. Anecdotal accounts of the similarity between NDEs and certain drug-induced altered states of consciousness prompted us to perform a large-scale comparative analysis of these experiences. After assessing the semantic similarity between ≈15,000 reports linked to the use of 165 psychoactive substances and 625 NDE narratives, we determined that the N-methyl-D-aspartate (NMDA) receptor antagonist ketamine consistently resulted in reports most similar to those associated with NDEs. Ketamine was followed by Salvia divinorum (a plant containing a potent and selective κ receptor agonist) and a series of serotonergic psychedelics, including the endogenous serotonin 2A receptor agonist N,N-Dimethyltryptamine (DMT). This similarity was driven by semantic concepts related to consciousness of the self and the environment, but also by those associated with the therapeutic, ceremonial and religious aspects of drug use. Our analysis sheds light on the long-standing link between certain drugs and the experience of "dying", suggests that ketamine could be used as a safe and reversible experimental model for NDE phenomenology, and supports the speculation that endogenous NMDA antagonists with neuroprotective properties may be released in the proximity of death.

[angelofthemornings]

Memantine might be an interesting option for me. Like the ones I was thinking about earlier, it's a drug for dementia, but it's being researched in bipolar patients with cognitive decline + it's used off label for autism patients to improve broad symptoms. So whether I have issues with bipolar decline or neurodivergency there's a chance of it working. It's an NMDA receptor antagonist like ketamine and I was just talking about it (ketamine) with my prescriber the other day because I really need to be on *some* kind of procognitive drug. (It wasn't a very productive conversation. She said Auvelity works the same way with less risk and I said "But that's got bupropion in it and my neurologist won't let me have that" and she was like, yeah, that sucks, doesn't it?)

[labru-ao3feed]

by Anonymous

When he locked eyes with Laios, something in his gut flipped. He took a step closer to the other man. He felt warm.

Something is wrong, Kabru thought in the back of his mind.

—

Kabru is separated from his party on the fourth floor of the dungeon. He encounters Laios for the first time, who claims to also have been separated. Something isn't right, but Kabru can't help but get closer...

Words: 3176, Chapters: 1/1, Language: English

Fandoms: ダンジョン飯 | Dungeon Meshi | Delicious in Dungeon

Rating: Explicit

Warnings: Rape/Non-Con

Categories: M/M, Other

Characters: Laios Touden, Kabru (Dungeon Meshi), Rinsha Fana

Relationships: Kabru/Laios Touden

Additional Tags: Succubi & Incubi, (specifically succubi), Cannibalism, (not exactly but adjacent—it's a succubus eating a human), Feelings Realization, post-coital regret, Submission, Submissive Character, Trans Kabru (Dungeon Meshi), MTNB Kabru (Dungeon Meshi), Nonbinary Kabru (Dungeon Meshi), Trans Laios Touden, FTM Laios Touden, Trans Male Laios Touden, Trans Male Character, Nonbinary Character, Pre-Relationship, Autistic Laios Touden, Submissive Kabru, Autistic Kabru (Dungeon Meshi)

[vanitas-vanitatum-mortis]

I remember talking with someone about it in 2019 or 2020 but why the hell is Anthony called Angel Dust?

And before you go and tell me the obvious, yes, I know he overdosed and went comatose. But he died in 1947. And PCP (phencyclidine - so called 'Angel Dust') was initially made in 1956 and used as anesthetic. It was used as a street drug in 1960's? 1970's? And Anthony was dead way before that.

The only reasons I see for this are:

- he overdosed something else but was very fond of PCP in Hell since it works as an NMDA receptor antagonist and it would help him escape reality he had to deal with

- Angel Dust was a "cool name" for a character being addicted to drugs that is literally living in Hell

- Vivzie just didn't take years into consideration and didn't know there would be people like me who would actually care about "some strange kind of accuracy"

- She somehow (probably) just didn't know about the year it was made, just how it works and that it was quite popular (mostly in United States).

Yes, I know most people don't give a shit. And it fits the character, don't get me wrong! I just still find this strange. Maybe because I dislike anachronistic things..?

I luv Anthony tho!!

[rustedskyprisms]

Tonight has also been very boring. I mean I figured; memantine is generally pretty boring (unless you’re taking a very strong dose, which, I kind of already missed my window and yeah I am aware that high doses of NMDA receptor antagonists do cause neurotoxicity (I’m not the most educated person on that area but I know it’s a thing)). The thing I like about it is how easy it makes physical movement.

[marchy-emmet]

According to me, after having a puff too much:

"Colress's EM waves can be compared to a NMDA receptor antagonist"

You know... like ketamine? That's what I said. That's what I actually said.

[k2spicespray]

Medical Uses Of Ketamine

Ketamine has several important medical uses, particularly in the fields of psychiatry and anesthesia. Here’s a breakdown of its key applications:

1. Treatment-Resistant Depression

Rapid Relief: Ketamine is known for its rapid antidepressant effects, often providing relief within hours, unlike traditional antidepressants which can take weeks.

Mechanism: It works primarily as an NMDA receptor antagonist, which helps increase glutamate levels and promotes neuroplasticity.

2. Anesthesia

Dissociative Anesthesia: Ketamine induces a trance-like state, providing analgesia and sedation without significantly depressing respiration, making it useful in surgical settings.

Pediatric Use: Commonly used in children due to its safety profile and ease of administration. Buy Ketamine in USA

3. Chronic Pain Management

Neuropathic Pain: Effective in treating conditions like fibromyalgia and complex regional pain syndrome (CRPS).

Infusion Therapy: Administered in low doses through infusions for sustained pain relief.

4. Post-Traumatic Stress Disorder (PTSD)

Symptom Reduction: Studies suggest ketamine can rapidly reduce PTSD symptoms, offering new hope for patients who have not responded to conventional treatments. Ketamine for sale in UK

5. Bipolar Disorder

Mood Stabilization: Some research indicates ketamine may help stabilize mood during depressive episodes in individuals with bipolar disorder.

6. Suicidal Ideation

Emergency Intervention: Ketamine has been shown to rapidly decrease suicidal thoughts in patients, making it a potential emergency treatment in acute situations.

7. Other Psychiatric Disorders

Anxiety Disorders: Emerging studies are exploring ketamine's effects on generalized anxiety disorder (GAD) and social anxiety.

Obsessive-Compulsive Disorder (OCD): Some evidence suggests it may be beneficial in reducing symptoms. Ketamine online

8. Research Applications

Neuroscience: Used in research to study brain function and the effects of depression and pain on neurobiology.

These diverse medical applications highlight ketamine's potential as a versatile treatment option, particularly in areas where traditional therapies have failed. Ongoing research continues to explore and expand its therapeutic uses.

[ohiopsychiatricservices121]

Medical How does the mechanism of action of esketamine nasal spray differ from traditional oral antidepressants?

Esketamine nasal spray differs from traditional oral antidepressants primarily in its mechanism of action. While most oral antidepressants, such as SSRIs and SNRIs, work by inhibiting the reuptake of serotonin and norepinephrine, esketamine primarily acts as an NMDA receptor antagonist. This action leads to an increase in glutamate release, which is thought to facilitate synaptic plasticity and promote rapid antidepressant effects.

For Ohio mental health services, this difference is significant because:

Rapid Onset: Esketamine can provide relief within hours, which is especially beneficial for patients experiencing acute suicidal ideation or severe depression. This contrasts with traditional antidepressants that often take weeks to show effects.

Treatment-Resistant Cases: Esketamine is particularly useful for patients who have not responded to multiple oral antidepressants, addressing a critical gap in treatment options within Ohio’s mental health framework.

https://ohiopsychiatricservices.com/esketamine/

[mental-health-solution]

Innovative Therapies for Depression | Relief Mental Health

Innovative therapies like transcranial magnetic stimulation (TMS) and SPRAVATO® are emerging as effective treatments for treatment-resistant depression and other diagnoses. These innovative therapies for depression offer new hope for those who have not responded to traditional treatments.

What is TMS? TMS is a non-invasive therapy that stimulates the nerve cells in the brain. It involves targeting magnetic fields at specific brain areas like the dorsolateral prefrontal cortex, which regulates things like your heart rate and mood. These pulses induce small electric currents that rewire the neuron patterns and alter dysfunctional brain patterns associated with depression. It’s this brain stimulation that brings about change.

TMS is FDA-approved for treating major depressive disorder and other diagnoses in individuals who have not responded adequately to traditional antidepressant medications. But it is often used off-label for treating ADHD, post-traumatic stress disorder and trauma, and more.

What is SPRAVATO®? SPRAVATO® is also FDA-approved for treating treatment-resistant depression. It’s a prescription medicine used along with an oral antidepressant. SPRAVATO® is an NMDA receptor antagonist and works rapidly by boosting glutamate, a neurotransmitter in the brain. This excites the cells in the brain and encourages memory and learning functions. It also encourages your brain to become comfortable with this new state, which helps fight the symptoms of depression.

[ptmasterguide]

Alzheimer's disease (Treatment and Management)

Alzheimer’s disease (Treatment and Management) While there is no cure for Alzheimer’s disease, treatments are available to manage symptoms and improve quality of life: Medications: Drugs like cholinesterase inhibitors (e.g., donepezil, rivastigmine, and galantamine) and NMDA receptor antagonists (e.g., memantine) can help manage symptoms, particularly in the early to moderate stages. Newer…

[credenceresearchdotblog]

The Neurodegenerative Disease market is projected to grow from USD 51,995 million in 2024 to USD 88,009.91 million by 2032, reflecting a compound annual growth rate (CAGR) of 6.8%.Neurodegenerative diseases, such as Alzheimer's, Parkinson's, Huntington's, and Amyotrophic Lateral Sclerosis (ALS), are chronic, progressive conditions characterized by the deterioration of neurons in the brain and spinal cord. These diseases significantly impair cognitive and motor functions, leading to severe disabilities and a reduced quality of life. The neurodegenerative disease market has gained substantial attention in recent years due to the increasing prevalence of these disorders, advancements in research, and the urgent need for effective therapies.

Browse the full report at https://www.credenceresearch.com/report/neurodegenerative-disease-market

Market Drivers

One of the primary drivers of the neurodegenerative disease market is the aging global population. As life expectancy increases, so does the incidence of age-related neurodegenerative conditions. According to the World Health Organization (WHO), the number of people aged 60 years and older is expected to double by 2050, leading to a significant rise in the prevalence of neurodegenerative diseases. This demographic shift is fueling demand for new treatments and driving market growth.

Another critical driver is the advancements in biotechnology and pharmaceutical research. Over the past decade, there has been considerable progress in understanding the molecular mechanisms underlying neurodegenerative diseases. Innovations in genomics, proteomics, and biomarker discovery are paving the way for more targeted and personalized therapies. Additionally, the development of novel drug delivery systems, such as nanoparticles and gene therapy, has opened new avenues for treating these complex conditions.

Market Segmentation

The neurodegenerative disease market can be segmented based on disease type, treatment type, and geography.

- Disease Type: The market is primarily categorized into Alzheimer's disease, Parkinson's disease, multiple sclerosis, Huntington's disease, and others. Alzheimer's disease holds the largest market share, driven by its high prevalence and the significant economic burden it imposes on healthcare systems.

- Treatment Type: Treatment options include pharmacological therapies, such as cholinesterase inhibitors, NMDA receptor antagonists, and dopamine agonists, as well as non-pharmacological interventions like physical therapy, cognitive training, and lifestyle modifications. In recent years, there has been growing interest in disease-modifying therapies that aim to slow or halt disease progression rather than merely alleviating symptoms.

- Geography: Geographically, the market is divided into North America, Europe, Asia-Pacific, Latin America, and the Middle East & Africa. North America dominates the market due to the presence of a well-established healthcare infrastructure, high healthcare expenditure, and significant investment in research and development. Europe follows closely, with a strong focus on research and collaboration among pharmaceutical companies, academic institutions, and government bodies.

Challenges and Opportunities

Despite the progress, the neurodegenerative disease market faces several challenges. One of the most significant obstacles is the high failure rate of clinical trials. Neurodegenerative diseases are complex, with multiple pathways involved in their pathogenesis. As a result, many potential treatments fail to demonstrate efficacy in late-stage clinical trials, leading to high development costs and lengthy timelines. This has created a cautious environment for investors and pharmaceutical companies, who are wary of the risks associated with drug development in this field.

However, these challenges also present opportunities. The unmet need for effective treatments is driving innovation and collaboration across the industry. Public-private partnerships, such as the Accelerating Medicines Partnership (AMP) in Alzheimer's Disease, are bringing together stakeholders from various sectors to share data, resources, and expertise. Additionally, the growing focus on precision medicine and the use of artificial intelligence (AI) in drug discovery are expected to accelerate the development of new therapies.

Future Outlook

The neurodegenerative disease market is poised for significant growth in the coming years. With the aging population, increasing awareness, and advancements in research, the demand for effective treatments will continue to rise. Companies that can successfully navigate the challenges of drug development and bring innovative therapies to market will likely see substantial returns on investment.

Moreover, as our understanding of the underlying mechanisms of neurodegenerative diseases deepens, the potential for breakthroughs in treatment becomes more promising. The integration of AI, big data, and personalized medicine into the research and development process is expected to revolutionize the way we approach these diseases, offering hope to millions of patients worldwide.

Key Player Analysis:

Novartis

Pfizer

Merck Serono

Biogen Idec

TEVA Pharmaceutical Industries

UCB

Boehringer Ingelheim

Sanofi

GlaxoSmithKline (GSK)

Hoffmann-La Roche Ltd.

Segmentations:

By Indication Type

Alzheimer’s Disease

Huntington Disease

Parkinson’s Disease

Multiple Sclerosis

Other Indication Types

By Drug Type

Dopamine Agonists

Cholinesterase Inhibitors

Immunomodulatory Drugs

N-methyl-D-aspartate Receptor Antagonists

Other Drug Types

By Region

North America

US

Canada

Mexico

Europe

Germany

France

UK

Italy

Spain

Rest of Europe

Asia Pacific

China

Japan

India

South Korea

South-east Asia

Rest of Asia Pacific

Latin America

Brazil

Argentina

Rest of Latin America

Middle East & Africa

GCC Countries

South Africa

Rest of Middle East and Africa

Browse the full report at https://www.credenceresearch.com/report/neurodegenerative-disease-market

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[eligalilei]

"I'm not convinced that anti-inflammatory strategies are going to turn out to be the most powerful treatments around," cautions Raison. "But I think if we really want to understand depression, we definitely have to understand how the immune system talks to the brain. I just don't think we've identified immune-based or anti-inflammatory treatments yet that are going to have big effects in depression."

http://www.npr.org/sections/health-shots/2015/10/25/451169292/could-depression-be-caused-by-an-infection?utm_source=facebook.com&utm_medium=social&utm_campaign=npr&utm_term=nprnews&utm_content=2050

So.... Just because aspirin doesn’t cure depression, we should can the inflammatory hypothesis? It seems to me that without a systems approach to depression that does not rely on a billiard-ball model of causality we will only ever be stalking ghosts.

Clearly a single ‘steersman’ marker has not been forthcoming, though IL-6, TNF-alpha and CRP have all been suggested as candidates.

It seems clear to me, being an explorer of the realms of sickness-behaviour myself, that whatever biological substratum depression may have, it is mirrored in and by the life-world and learns to take many masks.

Do you have chronic low-level inflammation, or did you have an abusive childhood? Inflammation, it is fair to say, I think, that though inflammation can pretty reliably cause depression, this is not to imply that if one decreases x inflammatory marker but fails to abolish depression, that it is fair to assume depression is not ‘caused’ by inflammation.

It seems from what I have seen, in most cases, that changing only lifestyle, exercise, diet &c. in isolation is insufficient, as a deeply entrenched homeostasis has already been reached. As Lacan states, we are not in therapy because we want to get well, but rather because our wanting is itself dysfunctional. Douglas Dailey refers to sickness behaviour as apoptosis of the self. In darker moments I’ve wondered if this controlled deletion of the individual is not a conserved behaviour because of its efficacy in trimming the herd of  unwanted resource-sinks. If sick people get needy and grumpful, their kin won’t feel as bad about ditching them in the woods to die.

“Very recently, we found that, at baseline, serum levels of IL-6 in the ketamine responder group were significantly higher than those of the control and non-responder groups [30]. In contrast, serum levels of IL-6 did not differ between control and non-responder groups. In addition, serum levels of TNF-α remained the same after ketamine infusion. These findings suggest serum IL-6 (not TNF-α) as a useful predictor for clinical outcome in patients with treatment-resistant MDD undergoing ketamine therapy [30]. The NMDA receptor antagonists such as ketamine may suppress Th1-type cytokines and shift the balance toward humoral immunity.”

[uptothetrendblogs]

Global Alzheimer’s Drugs Market

Global Alzheimer’s Drugs Market Seen Soaring ~11% Growth to Reach USD ~11.5 Billion  by 2032, Projects Univdatos Market Insights

According to a new report by Univdatos Market Insights, the global Alzheimer’s drugs market is expected to reach around USD 11.5 Billion in 2032 by growing at a CAGR of 11%. Alzheimer’s disease as disease presents a stiff nut to crack in the global health sector given the staggering numbers impacted and the unrelenting way it affects the human brain by causing progressive cognitive impairment. Being a disease that affects the elderly, both in terms of prevalence and incidence, Alzheimer’s disease has driven the development of pharmaceutical and healthcare businesses to step up the processes of finding and creating effective medicines to treat it.

Analysis of Global Demand for Alzheimer’s Drugs

There is, therefore, a higher demand for Alzheimer’s drugs and this is further driven by the elderly population which is experiencing the disease more than any other age group. Estimates from WHO state that around 50 million individuals globally are currently suffering from dementia, and it is common knowledge that Alzheimer’s disease contributes to most of these cases. Since there is a progressing problem with aging populations across the world, many people affected by Alzheimer’s will be even more numerous in the next few years, which will require effective drugs to be developed.

Dementia Prevalence Globally (data in Millions)

Unlock The Insights of This Strategic Report – https://univdatos.com/report/alzheimers-drugs-market/get-a-free-sample-form.php?product_id=62128

Alzheimer’s Drugs Cost Considerations

Some of the primary issues faced in the Alzheimer’s drugs market include the hefty expense incurred to cover costs of the drugs. Some Alzheimer’s drugs may be costly, so everyone, including the patient, loved ones, or the treating healthcare facility, may incur enormous expenses. The above drugs are relatively expensive because of the complexity of Alzheimer’s disease, the continuing need to research and to try and find new treatments, and because many of the drugs are not selective and have difficulties in targeting precisely the right mechanisms in the disease. There is an attempt to solve such cost-related issues; for instance, there are attempts to manufacture generic forms of some of the drugs used to treat the disease and there is a treatment program for implementing efficient costs.

Fig 1. Percentage Population Considering Cost of Accessing Treatment as Biggest Problem in Healthcare System:

Treatment Options

At present, the treatment of Alzheimer's disease is still confined to the use of drugs such as cholinesterase inhibitors and NMDA receptor antagonists that focus on symptom control and deceleration of the progression of the disease. These drugs have been proven to bring some hope of ameliorating the cognitive disorder and the quality of life of the affected Alzheimer patients. Although current therapies have been proven to partially ameliorate some of the symptoms of the disease and significantly extend life expectancy, there remains a huge demand for innovative therapeutic approaches that address the causes of the disease and may have curative potential.

There are new classes of drugs; monoclonal antibody and vaccine agents that are being synthesised to counter proteins and pro belongs to molecules that are believed to play a role in the cause of Alzheimer’s disease. Despite these limitations, these therapies offer hope that could lead to improved translation of diagnosis, prognosis, and treatment of Alzheimer’s patients. Current scientific studies conduct trials on the safety and efficacy of these promising therapies for the treatment of cancer to make them available to patients globally, shortly.

Recent Developments/Awareness Programs:- Several key players and governments are rapidly adopting strategic alliances, such as partnerships, or awareness programs for the treatment:-

In July 2023, The U.S. FDA granted regulatory approval for Leqembi (lecanemab-irmb) to treat Alzheimer’s disease.

In December 2022, Eisai Co. Ltd. and Washington University School of Medicine in St. Louis formed a research collaboration to develop new treatments for Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative conditions.

In March 2022,  Adlarity (donepezil hydrochloride), a cholinesterase inhibitor developed by Corium Inc., was approved by the U.S. FDA for treating patients with mild, moderate, or severe dementia of Alzheimer's type.

In March 2022, Eisai Co., Ltd. and Biogen Inc. amended their collaboration agreement. Through this, Eisai received a tiered royalty based on the net sales of ADUHELM rather than sharing global profits and losses.

In June 2021, Aduhelm (aducanumab) manufactured by Biogen Inc. was approved by the U.S. FDA using the accelerated approval pathway.

Unlock The Insights of This Strategic Report – https://univdatos.com/report/alzheimers-drugs-market/get-a-free-sample-form.php?product_id=62128

Conclusion

The global Alzheimer's drugs market is poised for growth, driven by the increasing demand for effective treatments and the development of innovative therapies. While cost considerations remain a challenge, efforts are underway to address these concerns and make Alzheimer's drugs more accessible and affordable. With continued research and development, the future looks promising for Alzheimer's patients, with the potential for more effective treatments that can improve quality of life and slow disease progression.

Key Offerings of the Report

Market Size, Trends, & Forecast by Revenue | 2024−2032F.

Market Dynamics – Leading Trends, Growth Drivers, Restraints, and Investment Opportunities

Market Segmentation – A detailed analysis by Type and End-User

Competitive Landscape – Top Key Vendors and Other Prominent Vendors

Author: Aman Sharma

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[rustedskyprisms]

TIL acetaminophen might be an NMDA receptor antagonist. The research papers relating to this are very much beyond my comprehension but that’s very interesting to me. It’s important to note that this does not mean it has any psychoactive effects.

[sparklyeevee]

Approximating Common OTC Combination Medicines With Non-Combination Meds

Contains notes on what each ingredient is meant to do, and the most common reasons you might want to avoid it.

Excedrin extra-strength or Excedrin Migraine (per usual 2 tablet dose)

One extra-strength (500mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1.5 regular aspirin (325mg), OR six "low dose" (81mg aspirin), OR one extra-strength or "back and body" aspirin (500mg). You're going for about 500mg but aspirin doses are arcane. NSAID pain reliever, fever reducer, antiinflammatory, salicylate, blood thinner, hard on the stomach.

2 cups of black or green tea OR one cup of brewed coffee OR a coffee drink with two shots of espresso OR 2tsp instant coffee crystals (you can turn it into liquid coffee or not) OR half a standard caffeine pill OR a 100mg caffeine pill if you can find them. 100-150mg of caffeine. Stimulant, vasoconstrictor, diuretic, increases heart rate, iirc works synergistically with the pain relievers.

Excedrin PM (per usual 2 tablet dose)

One extra-strength (500mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1.5 regular aspirin (325mg per tablet), OR six "low dose" (81mg aspirin per tablet), OR one extra-strength or "back and body" aspirin (500mg). You're going for about 500mg but aspirin doses are arcane. NSAID pain reliever, fever reducer, antiinflammatory, salicylate, blood thinner, hard on the stomach.

2 diphenhydramine hcl tablets (Benadryl, Sominex, or Unisom Sleep Gels) (25mg per tablet, 50mg total) - antihistamine, sleep aid, anticholinergic, dehydrating.

Note: Excedrin PM container 38mg per tablet of diphenhydramine citrate, not HCL. 25mg diphenhydramine hcl is equivalent. Diphenhydramine citrate is extraordinarily difficult to find outside of combination medicines. If for some reason you must have the citrate, do not take the aspirin and combine 1 extra strength acetaminophen with 2 tablets of combined ibuprofen (200mg) and diphenhydramine citrate (38mg), typically marketed as Advil pm or ibuprofen pm.

NyQuil (per typical 2 gel cap dose or 30ml of liquid medicine)

2 regular (325mg per tablet, 650mg total) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

2 gel caps (15mg each, 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 half tablet (25mg per tablet, 12.5mg total) doxylamine succinate (unisom sleep tabs) - sleep aid, antihistamine, anticholinergic, dehydrating.

Note 1: dextromethorphan by itself is a right pain to find these days. If you tolerate guaifenesin, a single tablet of 30mg dextromethorphan and 600mg guaifenesin will serve your purposes as well as or better than dextromethorphan by itself.

Note 2: Look, I fucking hate NyQuil, okay? It's terrible. Doxylamine succinate is an objectively worse drug than diphenhydramine unless you're specifically trying to sleep for 12+ hours, dextromethorphan is less useful without guaifenesin, and that's probably more acetaminophen than you need. My advice is to take 500mg acetaminophen (1 extra strength tablet), 1 tablet of combined dextromethorphan and guaifenesin (30/600, so the coughing you do anyway will be productive), and 25mg of diphenhydramine hcl (if you actually want the sleep aid).

NyQuil Severe

2 regular (325mg per tablet, 650mg total) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 or 2 gel caps (15mg each, 15 or 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 half tablet (25mg per tablet, 12.5mg total) doxylamine succinate (unisom sleep tabs) - sleep aid, antihistamine, anticholinergic, dehydrating.

1 tablet (15mg) pseudoephedrine - decongestant, mild stimulant, increases heart rate and blood pressure.

Note 1: see NyQuil above for notes on dextromethorphan and how much I hate NyQuil.

Note 2: Yeah I straight up replaced the phenylephrine with a different drug because oral phenylephrine doesn't work as a decongestant. This has been confirmed repeatedly. It doesn't fucking work. If you can't access, or can't take, pseudoephedrine, guaifenesin will help some, and so will maybe a warm cup of tea. If you insist on taking phenylephrine anyway, you're looking for a single 10mg tablet.

Note 3: this stuff contains 20mg dextromethorphan per dose, which doesn't seem to exist elsewhere. If you have a bad cough, take 2 15s, if you have a mild or occasional cough, take 1, if you don't have a cough, keep 1 handy but don't take it if you don't need it.

DayQuil (per 2 gelcaps or 30ml liquid)

2 regular (325mg per tablet, 650mg total) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 or 2 gel caps (15mg each, 15 or 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 tablet (15mg) pseudoephedrine - decongestant, mild stimulant, increases heart rate and blood pressure.

Note 1: see note 1 on NyQuil for more on dextromethorphan logistics, note 2 on NyQuil Severe for more on replacement of phenylephrine with pseudoephedrine, and note 3 on NyQuil Severe for even more dextromethorphan logistics.

DayQuil Severe

2 regular (325mg per tablet, 650mg total) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 or 2 gel caps (15mg each, 15 or 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 half tablet (600mg/tablet, 300mg total) guaifenesin - mucus thinner.

1 tablet (15mg) pseudoephedrine - decongestant, mild stimulant, increases heart rate and blood pressure.

Note 1: there's 400mg of guaifenesin in a normal dose of DayQuil Severe, but tablets below 600mg are hard to find. 600mg is probably fine. You can also replace the dextromethorphan gels and guaifenesin tablet with a whole or half tablet of dextromethorphan 30mg/guaifenesin 600mg.

See note 2 on NyQuil Severe for more on replacement of phenylephrine with pseudoephedrine, and notes 1 and 3 on NyQuil Severe for more on dextromethorphan logistics.

Pamprin Multi-Sympton Maximum Strength

One extra-strength (500mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 tablet (50mg) pamabrom (diurex) - diuretic, meant to treat bloating, apparently a xanthine and unsettlingly difficult to research, might not be a great idea if you're very sensitive to caffeine but honestly I couldn't say for sure.

1 tablet (4mg) chlorphenamine maleate - antihistamine, sedating, anticholinergic. The actual thing in Pamprin is pyrilamine maleate, but best I can tell that's not available by itself, and chlorphenamine seems to be the closest cousin. There's also no evidence that antihistamines actually help pms symptoms, so feel free to just skip it.

Pamprin Max Pain + Energy

One extra-strength (500mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1.5 regular aspirin (325mg), OR six "low dose" (81mg aspirin), OR one extra-strength or "back and body" aspirin (500mg). You're going for about 500mg but aspirin doses are arcane. NSAID pain reliever, fever reducer, antiinflammatory, salicylate, blood thinner, hard on the stomach.

2 cups of black or green tea OR one cup of brewed coffee OR a coffee drink with two shots of espresso OR 2tsp instant coffee crystals (you can turn it into liquid coffee or not) OR half a standard caffeine pill OR a 100mg caffeine pill if you can find them. 100-150mg of caffeine. Stimulant, vasoconstrictor, diuretic, increases heart rate, iirc works synergistically with the pain relievers.

Note: This is literally just Excedrin, pink edition. Also it contains 2 common allergens (red 40 and coconut oil) that Excedrin does not.

Midol Complete (per tablet)

One extra-strength (500mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 cup of black or green tea OR half a cup of brewed coffee OR a coffee drink with 1 shot of espresso OR 1tsp instant coffee crystals (you can turn it into liquid coffee or not) OR one quarter a standard caffeine pill OR a half 100mg caffeine pill if you can find them. 50-100 mg of caffeine. Stimulant, vasoconstrictor, diuretic, increases heart rate, iirc works synergistically with the pain relievers.

1 tablet (4mg) chlorphenamine maleate - antihistamine, sedating, anticholinergic. The actual thing in Midol Complete is pyrilamine maleate, but best I can tell that's not available by itself, and chlorphenamine seems to be the closest cousin. There's also no evidence that antihistamines actually help pms symptoms, so feel free to just skip it.

Coricidin HBP Cold and Flu (per 2 tablet dose)

Two regular (325 mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 tablet (4mg) chlorphenamine maleate - antihistamine, sedating, anticholinergic.

Coricidin HBP Cough and Cold

1 tablet (4mg) chlorphenamine maleate - antihistamine, sedating, anticholinergic.

2 gel caps (15mg each, 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

Note: dextromethorphan by itself is a right pain to find these days. If you tolerate guaifenesin, a single tablet of 30mg dextromethorphan and 600mg guaifenesin will serve your purposes as well as or better than dextromethorphan by itself.

Coricidin HBP Cough, Cold, and Flu

Two regular (325 mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

1 or 2 gel caps (15mg each, 15 or 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 half tablet (600mg/tablet, 300mg total) guaifenesin - mucus thinner.

Note 1: this stuff contains 20mg dextromethorphan per dose, which doesn't seem to exist elsewhere. If you have a bad cough, take 2 15s, if you have a mild or occasional cough, take 1, if you don't have a cough, keep 1 handy but don't take it if you don't need it.

Note 2: there's 400mg of guaifenesin in a normal dose of Coricidin Cough, Cold & Flu, but tablets below 600mg are hard to find. 600mg is probably fine. You can also replace the dextromethorphan gels and guaifenesin tablet with a whole or half tablet of dextromethorphan 30mg/guaifenesin 600mg.

Coricidin Nighttime

Two regular (325 mg) paracetamol/acetaminophen (Tylenol) - non-NSAID pain reliever and fever reducer, hard on liver.

2 gel caps (15mg each, 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 half tablet (25mg per tablet, 12.5mg total) doxylamine succinate (unisom sleep tabs) - sleep aid, antihistamine, anticholinergic, dehydrating.

Note 1: See note on Coricidin Cough and Cold for more on dextromethorphan logistics

Note 2: Please take 25mg diphenhydramine hcl instead of the doxylamine succinate.

Coricidin Chest Congestion and Cough

1 or 2 gel caps (15mg each, 15 or 30mg total) dextromethorphan - cough suppressant, nmda receptor antagonist, histaminergic for some people.

1 half tablet (600mg/tablet, 300mg total) guaifenesin - mucus thinner.

Note: strictly speaking, this is 2/3 of a tablet of dextromethorphan 30mg/guaifenesin 600mg, so if you're good at cutting pills that's another option.

I feel like I'm missing an entire category of combination meds here. Please let me know if there's something else on which you'd like to see this kind of breakdown.