Tesarossa
𝒀𝒐𝒖'𝒓𝒆 𝒔𝒖𝒄𝒉 𝒂 𝒔𝒕𝒓𝒂𝒏𝒈𝒆 𝒈𝒊𝒓𝒍
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The ONLY Skin Care Guide Youll EVER Need
Thread Song
Everything About Tretinoin
Everything About Ghkcu
Everything About ISOTRETINOIN (Accutane)
10 mg PO daily; may increase up to 20 mg/day after 1 week
10 mg PO daily; may increase up to 20 mg/day after 1 week; maintain at lowest effective dose and assess need of therapy periodically if extended therapy required
Everything You Should Know About Tazarotene
Tazarotene works through selective activation of nuclear retinoic acid receptors.
Key steps:
Downstream effects:
Because it is more selective (especially for RAR-β/γ, which are abundant in epidermis), it can be more potent than tretinoin in some studies but often more irritating.
It is sometimes used off-label for other keratinization disorders or as part of combination regimens (e.g., with topical corticosteroids for psoriasis).
How to use:
Very common (local):
These are usually dose- and vehicle-dependent and often improve after the first few weeks with proper moisturization and gradual introduction. Higher strengths (0.1%) cause more irritation than 0.05% or the 0.045% lotion.
Less common:
Serious / important:
Systemic side effects are rare because absorption is low when used as directed on limited areas.
Tazarotene is often chosen when stronger efficacy is needed (especially for thicker lesions or psoriasis) and the patient can tolerate more irritation. Adapalene is usually preferred for sensitive skin. Tretinoin remains the most studied for anti-aging.
Full Estriol Cream Guide
My End Of Guide Notes
Lol this took a long ass time of revision and testing.
I had to find out how to format correctly which took me hours and a failed thread, https://looksmax.org/threads/clenbuterol-the-adventurer-full-clen-guide.2326657/(Literally posted this blank and had to completely paste it google docs again in under 30 minutes)
I finally got the formatting correct in this guide below though which was sort of a test for this thread
Ive been making and revising this for a bit of while now because skin shit is already talked about a lot but i decided to lock in on it and make it a story.
Everyone LOVES my story guides.
Anyway Hope You Enjoyed
(EDIT):THE POINT OF THE SOURCES WAS SO I CAN SHOW YOU WHERE I GOT THE INFORMATION. WHY IS HE SO STUPID.
I ALSO USE DASHES IN LOTS OF MY REGULAR THREADS TOO
(Edit 2) I removed all unnecessary symbols
SOURCES: For the Info (NOT FOR THE PRODUCTS)
www.mayoclinic.org
www.academicallderm.com
pimpl.com
www.perfectb.com
pmc.ncbi.nlm.nih.gov
#VolpaMogs
(Giveaways over but maybe i can win in spirit
)
TABLE OF CONTENT
This guide will contain the following:Stories(Giant Part of my Guides) In-Depth Guides, Application/Dosing Videos, Summaries, Dosing, Pathways, Images, Basically EVERYTHING You Could Ask For.
I've made the summaries and stories incase you didn't want to read the In-Depth Guides, because they are ridiculously long
Thread Song
Everything About Tretinoin
Tret used to be a loyal knight in the Crystal Castle. He protected the royal skin with his shiny golden armor. But the strict rules and heavy oils made him restless. One night he took off his special badge, called himself a rogue knight, and snuck out the back gate. He carried only his glowing blade and pure purpose. The old guards yelled that a real warrior never leaves the castle. Tret just smiled. He was tired of fixing the surface while deeper problems stayed hidden.
Outside the walls the land was dark and rough. He crossed the Valley of Congestion, where sticky black spots grew like thorns. He fought the hot Ironclad Flare that tried to burn him. Every morning his armor peeled and grew back stronger and smoother. People talked about the strange knight who made scars fade and rough ground turn firm.
Tret kept going. He learned that real change needs patience, nightly care, and the bravery to face the sun without hiding.
At last he stood on a high hill looking at clear, strong new land. The castle still shone far behind him, but Tret did not miss it. He had become the Rogue Knight—not fully part of the castle and not lost in the wild. His quiet journey showed everyone that strength does not come from staying perfect forever. It comes from peeling away the old and rising new under open skies.
Outside the walls the land was dark and rough. He crossed the Valley of Congestion, where sticky black spots grew like thorns. He fought the hot Ironclad Flare that tried to burn him. Every morning his armor peeled and grew back stronger and smoother. People talked about the strange knight who made scars fade and rough ground turn firm.
Tret kept going. He learned that real change needs patience, nightly care, and the bravery to face the sun without hiding.
At last he stood on a high hill looking at clear, strong new land. The castle still shone far behind him, but Tret did not miss it. He had become the Rogue Knight—not fully part of the castle and not lost in the wild. His quiet journey showed everyone that strength does not come from staying perfect forever. It comes from peeling away the old and rising new under open skies.
Tret speeds up how fast your skin cells turn over. It pushes out old, dead stuff, unclogs pores, and helps clear acne. Over time it builds more collagen so skin looks smoother and firmer, and it fades dark spots and fine lines. At first it can make your skin dry, red, and peel, but that usually settles once your skin gets used to it.
Tretinoin (all trans retinoic acid / ATRA) is the biologically active form of vitamin A. It is a first generation prescription retinoid used primarily for acne vulgaris and photoaging (fine wrinkles, texture, dyspigmentation). Unlike over the counter retinol or retinaldehyde, it needs no enzymatic conversion in the skin and binds nuclear receptors directly.
This is a science based overview of its pathways, effects, practical use, and limitations. It is not medical advice consult a dermatologist for personalized recommendations, especially regarding pregnancy, skin type, or concurrent conditions.
Tretinoin acts as a ligand for nuclear receptors in the steroid/thyroid hormone receptor superfamily. The core pathway is:
This regulates hundreds of genes involved in differentiation, proliferation, apoptosis, inflammation, and extracellular matrix remodeling. Effects cascade beyond direct RARE genes.
Key downstream pathways and clinical effects:
UV exposure activates MAP kinase > c-Jun phosphorylation > AP-1 > MMP induction (collagen breakdown). Tretinoin pretreatment blocks much of this.
Tretinoin has relatively non-selective affinity for RAR subtypes (unlike adapalene’s preference for β/γ or trifarotene’s high γ-selectivity). RAR-γ predominance in epidermis drives both efficacy and irritation.
Result timelines: Acne improvements often begin in 2–6+ weeks (possible initial flare); photoaging changes require 3–6+ months of consistent use. Histologic collagen changes can appear earlier.
Formulations & strengths (common): Creams (0.025%, 0.05%, 0.1%), gels (including microsphere for slower release), lotions. Lower concentrations and vehicle choice affect irritation. Start low (often 0.025%).
Application principles (“low and slow”):
Retinization period: Temporary dryness, redness, peeling, stinging, or acne flare (weeks 1–4+). This is expected as turnover accelerates and usually improves with continued careful use + moisturization. Do not over-apply or escalate frequency too quickly.
Common (local, usually transient): Erythema, dryness, peeling, burning/stinging, irritation, photosensitivity, temporary pigment changes.
Less common: More severe irritation, contact dermatitis, or paradoxical worsening if overused.
Long-term: Generally safe and well-studied; no clear evidence of accelerated aging or major safety signals with appropriate use.
This is a science based overview of its pathways, effects, practical use, and limitations. It is not medical advice consult a dermatologist for personalized recommendations, especially regarding pregnancy, skin type, or concurrent conditions.
Molecular Pathways and Mechanism of Action
Tretinoin acts as a ligand for nuclear receptors in the steroid/thyroid hormone receptor superfamily. The core pathway is:
- Cellular entry and transport: Tretinoin enters keratinocytes and fibroblasts. Cytosolic cellular retinoic acid binding proteins (especially CRABP-II) help transport it to the nucleus and can modulate local bioavailability.
- Receptor binding: It binds retinoic acid receptors (RARs: α, β, γ). In human epidermis, RAR-γ is the dominant isoform (87–90% of RARs); RAR-α is also present, while RAR-β is more dermal or inducible. It forms heterodimers with retinoid X receptors (primarily RXR-α in skin).
- DNA binding and gene regulation: The RAR/RXR heterodimer binds retinoic acid response elements (RAREs, often DR5 sequences) in target gene promoters.
This regulates hundreds of genes involved in differentiation, proliferation, apoptosis, inflammation, and extracellular matrix remodeling. Effects cascade beyond direct RARE genes.
Key downstream pathways and clinical effects:
| Pathway / Effect | Mechanism | Main Clinical Outcome |
|---|---|---|
| Keratinocyte normalization | Alters proliferation/differentiation; reduces cohesion; promotes desquamation | Prevents microcomedones comedolytic; normalizes follicular epithelium (acne) |
| Anti-inflammatory | Inhibits AP-1 (Jun/Fos) transcription factor; downregulates TLR-2 reduces cytokines (e.g., IL-6, TNF-α), iNOS, leukocyte migration | Reduces inflammatory acne lesions; some benefit in other inflammatory conditions |
| Collagen & matrix | Upregulates COL1A1/COL3A1 (procollagen I & III) in fibroblasts; inhibits UV-induced MMPs (especially MMP-1, also -3/-8/-9) via AP-1 blockade | Increases dermal collagen; reduces degradation; improves fine wrinkles, elasticity, photoaging |
| Pigmentation | Accelerates epidermal turnover (melanin dispersal); possible indirect tyrosinase effects | Fades post inflammatory hyperpigmentation, some melasma/solar lentigines |
| Other | Fibroblast activation; possible effects on glycosaminoglycans/hydration; barrier modulation | Improved texture, thickness of epidermis over time |
UV exposure activates MAP kinase > c-Jun phosphorylation > AP-1 > MMP induction (collagen breakdown). Tretinoin pretreatment blocks much of this.
Tretinoin has relatively non-selective affinity for RAR subtypes (unlike adapalene’s preference for β/γ or trifarotene’s high γ-selectivity). RAR-γ predominance in epidermis drives both efficacy and irritation.
Clinical Uses
- Acne vulgaris (FDA-approved 1971): First-line for comedonal and inflammatory acne; prevents new lesions by targeting microcomedones. Often combined with benzoyl peroxide or antibiotics.
- Photoaging / photodamage (adjunctive indication, e.g., Renova): Strongest evidence among topicals for fine rhytides, texture, and dyspigmentation with long-term use (months).
- Off-label or supportive: Hyperpigmentation, some scarring, keratinization disorders; limited data for other uses.
- Oral tretinoin is used for acute promyelocytic leukemia (different mechanism involving PML-RAR-α degradation)—not relevant to topical skin use.
Result timelines: Acne improvements often begin in 2–6+ weeks (possible initial flare); photoaging changes require 3–6+ months of consistent use. Histologic collagen changes can appear earlier.
Practical Use Guide
Formulations & strengths (common): Creams (0.025%, 0.05%, 0.1%), gels (including microsphere for slower release), lotions. Lower concentrations and vehicle choice affect irritation. Start low (often 0.025%).
Application principles (“low and slow”):
- Apply at night only (light-sensitive).
- Cleanse gently; wait until skin is fully dry (15–30 min) to reduce irritation.
- Pea sized amount for the entire face; dab on forehead/cheeks/chin then spread thinly. Avoid eyes, lips, nostrils initially.
- Start 2–3 nights/week → every other night → nightly as tolerated over weeks to months.
- Buffering (“sandwich”): Moisturizer → wait → tretinoin → moisturizer (especially early on).
- Morning: Gentle cleanser + moisturizer + broad-spectrum SPF 30+ daily (non-negotiable; increased photosensitivity).
- Avoid concurrent strong actives (AHAs/BHAs, high-strength vitamin C, physical scrubs) on tretinoin nights until tolerant.
Retinization period: Temporary dryness, redness, peeling, stinging, or acne flare (weeks 1–4+). This is expected as turnover accelerates and usually improves with continued careful use + moisturization. Do not over-apply or escalate frequency too quickly.
Side Effects and Precautions
Common (local, usually transient): Erythema, dryness, peeling, burning/stinging, irritation, photosensitivity, temporary pigment changes.
Less common: More severe irritation, contact dermatitis, or paradoxical worsening if overused.
Long-term: Generally safe and well-studied; no clear evidence of accelerated aging or major safety signals with appropriate use.
Dosage
Your skin can only absorb a pea sized drop of tret per-day so any more is not needed.
Everything About Ghkcu
GHK-Cu was a strong warrior born from the bond of copper and three simple amino acids. He entered the human body with a clear mission: repair damage, rebuild strength, and restore order. From the moment he arrived, the body tested him. Inflammation rose like angry storms, free radicals attacked without warning, and old scars tried to hold their ground. Still, GHKCu stood firm, ready to fight for healthier skin and tissue.
His hardest battles came deep inside the damaged areas. Collagen had grown weak and broken. Blood vessels were slow to form. Cells that should have healed stayed stuck in chaos. GHK-Cu pushed through the pain of constant resistance, calling more repair cells to the fight and forcing the body to build stronger structures. Every time the body tried to age or break down, he met the challenge with steady force, never backing away even when progress felt slow.
In time, the strong warrior proved his worth. Wounds closed cleaner, skin grew firmer, and the signs of damage began to fade. GHK-Cu did not claim final victory, because the human body is always changing. But he remained a loyal fighter, ready for the next hardship, turning struggle into quiet strength and leaving the body better than he found it.
His hardest battles came deep inside the damaged areas. Collagen had grown weak and broken. Blood vessels were slow to form. Cells that should have healed stayed stuck in chaos. GHK-Cu pushed through the pain of constant resistance, calling more repair cells to the fight and forcing the body to build stronger structures. Every time the body tried to age or break down, he met the challenge with steady force, never backing away even when progress felt slow.
In time, the strong warrior proved his worth. Wounds closed cleaner, skin grew firmer, and the signs of damage began to fade. GHK-Cu did not claim final victory, because the human body is always changing. But he remained a loyal fighter, ready for the next hardship, turning struggle into quiet strength and leaving the body better than he found it.
GHK-Cu is a small, naturally occurring copper peptide that delivers bioavailable copper and broadly resets gene expression toward regenerative, anti inflammatory, and matrix remodeling programs. It has solid preclinical support for wound healing and ECM improvement, plus encouraging topical human data for skin quality. Injectable use is of growing interest but lacks rigorous human dose-finding and long-term safety trials.
GHK-Cu (glycyl-L-histidyl-L-lysine copper complex / copper tripeptide-1) is a naturally occurring copper binding tripeptide. It is one of the most studied regenerative peptides in skin and tissue research.
This guide covers its chemistry, mechanisms/pathways, effects, administration routes (including injection), dosing patterns reported in research and practice, safety, and evidence limitations. It is for informational purposes only. GHK-Cu is not FDA-approved as an injectable drug for systemic use. Injectable forms are largely research chemicals or compounded; consult a qualified healthcare professional before any use.
Copper transport & enzymatic supportIt acts as a copper ionophore/shuttle. It can take copper from albumin and deliver it in a non toxic form to cells. This supports copper-dependent enzymes such as:
Key downstream pathways and effects:
Human topical studies (creams/gels at 0.05–0.1% or higher) have shown improvements in skin firmness, elasticity, wrinkles, and collagen density in some trials. Injectable systemic effects in humans lack controlled clinical trial data.
Injectable (subcutaneous – experimental/research)Used in research settings and by some compounding pharmacies or peptide communities. No large, rigorous human pharmacokinetic or dose-finding trials exist for systemic injection. Effects are extrapolated from animal data, topical results, and anecdotal/clinic reports.
Other routes (microneedling, mesotherapy for scalp, experimental oral) exist but have even less standardized data.
Injectable
Injectable: Safety data are limited. No large controlled human trials tracking adverse events for systemic use. Reported effects are mostly mild and local:
Long term systemic safety is essentially unstudied in controlled trials.
This guide covers its chemistry, mechanisms/pathways, effects, administration routes (including injection), dosing patterns reported in research and practice, safety, and evidence limitations. It is for informational purposes only. GHK-Cu is not FDA-approved as an injectable drug for systemic use. Injectable forms are largely research chemicals or compounded; consult a qualified healthcare professional before any use.
1. What Is GHK-Cu?
- Structure: The tripeptide Gly-His-Lys tightly binds one copper(II) ion (binding constant 10¹⁶). The copper is essential for most of its biological activity.
- Natural occurrence: Found in human plasma, saliva, and urine. Plasma levels decline with age (roughly 200 ng/mL in young adults → 80 ng/mL by age 60). It is released during tissue breakdown (e.g., from collagen or SPARC protein) and acts as a local signal for repair.
- Discovery: Isolated in the 1970s by Loren Pickart as a factor that made aged liver tissue behave more like young tissue.
2. Core Mechanisms and Pathways
GHK-Cu works through dual, overlapping actions: copper delivery and gene signaling.Copper transport & enzymatic supportIt acts as a copper ionophore/shuttle. It can take copper from albumin and deliver it in a non toxic form to cells. This supports copper-dependent enzymes such as:
- Lysyl oxidase (LOX) — cross-links collagen and elastin
- Superoxide dismutase (SOD) — antioxidant defense
- Cytochrome c oxidase — mitochondrial energy production
Key downstream pathways and effects:
- Extracellular matrix (ECM) remodeling: Stimulates synthesis of collagen types I and III (and sometimes IV), elastin, decorin (organizes collagen fibrils and modulates TGF-β), and glycosaminoglycans (dermatan/chondroitin sulfate). It also regulates matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) in a balanced way — promoting removal of damaged matrix while limiting excessive breakdown.
- Anti-inflammatory: Suppresses NF-κB signaling, reduces TNF-α, IL-6, IL-1β, and other pro-inflammatory cytokines. Can reduce p38 MAPK activation in some models.
- Antioxidant: Increases SOD activity, reduces reactive oxygen species, and protects against oxidative and UV damage in cell and animal models.
- Angiogenesis: Upregulates VEGF and supports endothelial cell migration/proliferation, aiding new blood vessel formation (important for wound healing).
- Other signaling: Influences TGF-β/Smad, MAPK (ERK/p38), and PI3K/Akt pathways in various studies. Shows chemotactic effects (attracts repair cells) and possible effects on stem/progenitor cell behavior. Some data suggest proteasome/ubiquitin system activation (cellular cleanup) and DNA-repair gene upregulation.
3. Biological and Clinical Effects (Evidence Summary)
Most robust data are from cell culture, animal models, and topical human studies.| Effect | Main Evidence | Notes |
|---|---|---|
| Collagen & ECM increase | Strong (in vitro + some human topical) | Types I/III collagen, elastin, decorin, GAGs |
| Wound healing acceleration | Strong (animal + limited human dressings) | Faster closure, better organization, less scarring in models |
| Anti-inflammatory | Moderate–strong (preclinical) | Reduced cytokines and NF-κB |
| Antioxidant / protective | Moderate (preclinical) | SOD increase, ROS reduction |
| Skin quality (firmness, wrinkles, thickness) | Moderate (topical human trials) | Improvements reported in facial studies |
| Hair follicle support | Limited (in vitro + some topical) | Follicle elongation and papilla cell effects in culture |
| Systemic/regenerative (lung, gut, etc.) | Preclinical only | Interesting gene-reset data in COPD fibroblasts and other models; no strong human confirmation |
Human topical studies (creams/gels at 0.05–0.1% or higher) have shown improvements in skin firmness, elasticity, wrinkles, and collagen density in some trials. Injectable systemic effects in humans lack controlled clinical trial data.
4. Administration Routes
Topical (best-studied and most accessible)Used in serums, creams, and gels (often labeled Copper Tripeptide-1). Concentrations commonly 0.05–2%. Applied 1–2 times daily. Penetration is limited; some formulations use delivery systems to improve it. Strongest safety and efficacy track record.Injectable (subcutaneous – experimental/research)Used in research settings and by some compounding pharmacies or peptide communities. No large, rigorous human pharmacokinetic or dose-finding trials exist for systemic injection. Effects are extrapolated from animal data, topical results, and anecdotal/clinic reports.
Other routes (microneedling, mesotherapy for scalp, experimental oral) exist but have even less standardized data.
5. Dosing Information
TopicalTypical researched concentrations: 0.05–0.1% (sometimes higher in commercial products). Applied once or twice daily for 8–12+ weeks in studies.Injectable
- Conservative/research-community ranges often cited: 100–300 mcg once daily, or 1–3 mg per injection 2–3 times per week.
- Some protocols use 0.5–2 mg daily or every other day; loading phases of 2–5 mg 2-3×/week for 4–6 weeks followed by lower maintenance.
6. Safety and Side Effects
Topical: Excellent long-term safety record in cosmetics (decades of use). Mild, transient irritation, redness, or stinging is uncommon. Rare copper-related temporary greenish-blue tint or contact sensitivity. Generally well tolerated.Injectable: Safety data are limited. No large controlled human trials tracking adverse events for systemic use. Reported effects are mostly mild and local:
- Injection-site redness, itching, swelling, or bruising
- Occasional mild headache, fatigue, or metallic taste
Long term systemic safety is essentially unstudied in controlled trials.
Thread Song 2
(assuming the first is done)
(assuming the first is done)
Everything About ISOTRETINOIN (Accutane)
Isotret moved through the crowded city of the Skin like a shadow. He was a skilled pickpocketer, quiet and precise, targeting only the greediest targets. His specialty was the overstuffed oil glands , spilling sebum everywhere and feeding the rowdy acne gangs. With quick fingers he slipped past their defenses, lifted their excess oil, and left them smaller, quieter, and far less dangerous than before.
Night after night he worked the same streets. He picked the pockets of clogged pores, stealing the sticky buildup that kept new troublemakers locked inside. He emptied the wallets of angry red nodules until they shrank and lost their fight. The more he stole, the drier and calmer the city became. Some residents complained about the sudden lack of moisture on their lips and skin, but most were grateful that the constant chaos had finally begun to settle.
By the end of his long run, the once noisy districts stood clearer and quieter than they had in years. Isotret never claimed to be a hero. He was just a pickpocketer who specialized in taking what the body no longer needed. When his work was done, he slipped away, leaving behind a city that finally had room to heal.
Night after night he worked the same streets. He picked the pockets of clogged pores, stealing the sticky buildup that kept new troublemakers locked inside. He emptied the wallets of angry red nodules until they shrank and lost their fight. The more he stole, the drier and calmer the city became. Some residents complained about the sudden lack of moisture on their lips and skin, but most were grateful that the constant chaos had finally begun to settle.
By the end of his long run, the once noisy districts stood clearer and quieter than they had in years. Isotret never claimed to be a hero. He was just a pickpocketer who specialized in taking what the body no longer needed. When his work was done, he slipped away, leaving behind a city that finally had room to heal.
Isotretinoin remains the gold standard systemic therapy for severe or scarring acne because it uniquely induces sebocyte apoptosis, shrinks oil glands, normalizes keratinization, and reduces inflammation. Its benefits are linked to p53/FoxO-driven transcriptional programs that also explain many of its side effects. With proper patient selection, monitoring, and adherence to pregnancy-prevention programs, it offers the highest chance of long-term clearance among available treatments.
Always work with a dermatologist experienced in isotretinoin management. Individual dosing, monitoring, and risk assessment must be personalized.
Always work with a dermatologist experienced in isotretinoin management. Individual dosing, monitoring, and risk assessment must be personalized.
Accutane (isotretinoin / 13-cis-retinoic acid) is an oral retinoid and the most effective systemic treatment for severe, nodular, or treatment-resistant acne. It is the only medication that targets all four major pathogenic factors of acne at once.
This is a full in-depth guide covering chemistry, mechanisms/pathways, dosing, efficacy, monitoring, side effects, and practical considerations
Isotretinoin has relatively low direct affinity for nuclear retinoic acid receptors (RARs) and retinoid X receptors (RXRs). It acts largely as a prodrug: it undergoes intracellular isomerization (especially in sebocytes) to all-trans retinoic acid (ATRA) and other active metabolites (including 4-oxo metabolites). These bind RARs (primarily α and γ) and drive transcriptional changes. Some effects appear RAR-independent.
Four major actions (the reason it is uniquely effective):
Broader transcriptional impactIsotretinoin/ATRA signaling upregulates pro apoptotic and differentiation genes while downregulating pathways involved in lipogenesis, proliferation, and inflammation (including effects on androgen receptor, IGF-1/PI3K-AKT-mTOR, and PPAR signaling via FoxO proteins). These same pathways help explain both therapeutic benefits and many side effects (including teratogenicity via neural-crest cell apoptosis).
Sebaceous gland involution begins within 1 2 weeks and becomes pronounced by 8 weeks. Many patients experience continued improvement for weeks to months after stopping the drug.
Standard regimen (most common):
Higher doses: Up to 2 mg/kg/day may be used for very severe, scarring, or truncal acne (as tolerated).
Lower-dose / alternative regimens: Used for milder cases, better tolerability, or longer courses; may reduce side effects but can increase relapse risk if cumulative exposure is too low.
Administration notes:
Very common (dose related):Cheilitis (dry, cracked lips – nearly universal), dry skin, dry eyes/nose, nosebleeds, dermatitis, photosensitivity.
Common:Musculoskeletal pain/arthralgia, headache, elevated triglycerides/cholesterol, mild transaminase elevations, temporary hair thinning.
Less common / important:
This is a full in-depth guide covering chemistry, mechanisms/pathways, dosing, efficacy, monitoring, side effects, and practical considerations
1. What Is Isotretinoin?
- Chemistry: A synthetic first-generation retinoid and stereoisomer of all-trans retinoic acid (tretinoin).
- Brand names: Accutane (original, discontinued in many markets), Absorica, Claravis, Amnesteem, Sotret, Zenatane, and generics.
- Indications: Severe recalcitrant nodular acne unresponsive to conventional therapy (including systemic antibiotics). Also used off-label for moderate acne with scarring risk, significant psychosocial burden, or frequent relapse.
- Key property: Highly teratogenic (causes severe birth defects). Strict pregnancy prevention is mandatory.
2. Mechanisms of Action and Pathways
Isotretinoin has relatively low direct affinity for nuclear retinoic acid receptors (RARs) and retinoid X receptors (RXRs). It acts largely as a prodrug: it undergoes intracellular isomerization (especially in sebocytes) to all-trans retinoic acid (ATRA) and other active metabolites (including 4-oxo metabolites). These bind RARs (primarily α and γ) and drive transcriptional changes. Some effects appear RAR-independent.
Four major actions (the reason it is uniquely effective):
- Sebum suppression (most important)Dramatically shrinks sebaceous glands (often 70–90% reduction in size and sebum output). This is driven by induction of apoptosis (programmed cell death) in sebocytes and depletion of sebocyte progenitor cells.
- Key molecular mediators: Upregulation of p53, FoxO1, and FoxO3 transcription factors > induction of TRAIL (TNF-related apoptosis-inducing ligand), NGAL/lipocalin-2, and other pro-apoptotic proteins >caspase activation and cell death.
- Also causes cell-cycle arrest ( p21, cyclin D1).
- Normalization of follicular keratinizationReduces hyperkeratinization and cohesiveness of corneocytes in the follicle, helping prevent microcomedone formation (comedolytic effect). Linked in part to p53/FoxO1-driven changes (e.g., GATA6 regulation).
- Anti-inflammatory effectsDecreases inflammatory cytokines and innate immune signaling in the pilosebaceous unit. Indirectly reduces Cutibacterium acnes by starving the bacteria of sebum.
- Indirect antimicrobial effectLower sebum production creates a less favorable environment for C. acnes colonization.
Broader transcriptional impactIsotretinoin/ATRA signaling upregulates pro apoptotic and differentiation genes while downregulating pathways involved in lipogenesis, proliferation, and inflammation (including effects on androgen receptor, IGF-1/PI3K-AKT-mTOR, and PPAR signaling via FoxO proteins). These same pathways help explain both therapeutic benefits and many side effects (including teratogenicity via neural-crest cell apoptosis).
Sebaceous gland involution begins within 1 2 weeks and becomes pronounced by 8 weeks. Many patients experience continued improvement for weeks to months after stopping the drug.
3. Dosing
Standard regimen (most common):
- Start at 0.5 mg/kg/day, then increase to 0.5–1 mg/kg/day (divided into two doses with food) as tolerated.
- Typical course: 15–20 weeks.
- Goal for many clinicians: Treat until clear + 1 additional month, or aim for a cumulative dose of approximately 120–150 mg/kg (some evidence supports higher cumulative exposure, e.g., up to 220 mg/kg, for lower relapse risk in certain patients).
Higher doses: Up to 2 mg/kg/day may be used for very severe, scarring, or truncal acne (as tolerated).
Lower-dose / alternative regimens: Used for milder cases, better tolerability, or longer courses; may reduce side effects but can increase relapse risk if cumulative exposure is too low.
Administration notes:
- Take with food (especially fatty food) for better absorption (except certain micronized formulations like Absorica LD that have improved bioavailability).
- Once daily dosing is generally not recommended for standard capsules.
- A second course can be considered >2 months after the first if needed.
4. Efficacy and Outcomes
- Clears or markedly improves severe acne in the large majority of patients.
- Long term remission or cure after a single course in roughly 60–80% of patients (rates vary by study, dose, and patient factors).
- Reduces scarring risk by rapidly controlling severe inflammatory disease.
- Follow-up: Lipids and LFTs at 1–2 months (or when peak dose is reached); then as clinically indicated. Monthly pregnancy testing for those who can become pregnant.
- Additional tests (CBC, glucose, CK, etc.) based on individual risk factors.
6. Side Effects and Safety
Very common (dose related):Cheilitis (dry, cracked lips – nearly universal), dry skin, dry eyes/nose, nosebleeds, dermatitis, photosensitivity.
Common:Musculoskeletal pain/arthralgia, headache, elevated triglycerides/cholesterol, mild transaminase elevations, temporary hair thinning.
Less common / important:
- Mood changes, depression, or rare reports of suicidal ideation (causal link remains debated; monitor closely, especially in those with psychiatric history).
- Elevated creatine kinase, rare pancreatitis (with severe hypertriglyceridemia).
- Decreased night vision, corneal opacities, or idiopathic intracranial hypertension (rare).
- Possible temporary effects on bone/growth in adolescents with prolonged high-dose use.
- Theoretical concerns about inflammatory bowel disease have not been strongly supported by recent evidence
7. Practical Considerations
- Start low and titrate to minimize initial flares and side effects.
- Aggressive moisturization, lip balm, artificial tears, and sunscreen are essential.
- Avoid concurrent tetracyclines (risk of intracranial hypertension), excess vitamin A, and elective procedures that affect skin barrier during/soon after treatment.
- Alcohol and high-fat diets can worsen lipid elevations.
- Quality-of-life improvement is often dramatic once acne clears.
Dosage Forms & Strengths
tablet
- 5mg
- 10mg
- 20mg
capsule
- 15mg
oral solution
- 5mg/5mL
Major Depressive Disorder
Indicated for acute and maintenance treatment of major depressive disorder (MDD)10 mg PO daily; may increase up to 20 mg/day after 1 week
Generalized Anxiety Disorder
Indicated for acute treatment of generalized anxiety disorder (GAD)10 mg PO daily; may increase up to 20 mg/day after 1 week; maintain at lowest effective dose and assess need of therapy periodically if extended therapy required
Everything You Should Know About Tazarotene
Tazarotene moved through the city of the Skin like a silent ninja. Cloaked in precision, he struck only the targets that mattered. Clogged pores, thick rough patches, and stubborn acne strongholds. He never wasted a move. Where others fought loudly, Taz slipped in quietly, binding to his chosen receptors and forcing the skin cells to obey a stricter code.
At first the city resisted. His sharp techniques caused dryness, peeling, and temporary chaos as old layers were cut away. Some areas stung under his discipline. But the ninja did not hesitate. Night after night he returned, clearing blockages, calming inflamed zones, and training the skin to renew itself faster and cleaner than before.
When his mission was complete, the streets stood smoother and more ordered. The worst threats had been neutralized. Tazarotene, the focused ninja, vanished as quietly as he had arrived. leaving behind a stronger, clearer city that finally followed a better path.
At first the city resisted. His sharp techniques caused dryness, peeling, and temporary chaos as old layers were cut away. Some areas stung under his discipline. But the ninja did not hesitate. Night after night he returned, clearing blockages, calming inflamed zones, and training the skin to renew itself faster and cleaner than before.
When his mission was complete, the streets stood smoother and more ordered. The worst threats had been neutralized. Tazarotene, the focused ninja, vanished as quietly as he had arrived. leaving behind a stronger, clearer city that finally followed a better path.
Tazarotene is a potent, receptor-selective topical retinoid that normalizes skin cell behavior through RAR-β/γ activation and gene regulation (including TIG genes and AP-1 antagonism). It is highly effective for acne and plaque psoriasis and useful for photoaging, but it tends to cause more irritation than adapalene or lower-strength tretinoin. Success depends on proper introduction, moisturization, and sun protection. It is contraindicated in pregnancy.
What Is Tazarotene?
- Chemistry: An acetylenic retinoid (ethyl 6-[(4,4-dimethylthiochroman-6-yl)ethynyl]nicotinate). It is a prodrug.
- Active form: Rapidly converted in the skin by esterases to tazarotenic acid, the biologically active metabolite.
- Generation: Third-generation (polyaromatic) retinoid, designed for greater receptor selectivity than first-generation agents like tretinoin.
- Brand names / formulations:
- Tazorac (cream/gel 0.05% and 0.1%)
- Fabior (foam 0.1%)
- Arazlo (lotion 0.045%)
- Avage (cream 0.1% for photoaging)
- Generics available
2. Mechanism of Action and Pathways
Tazarotene works through selective activation of nuclear retinoic acid receptors.
Key steps:
- Converted to tazarotenic acid in the skin.
- Tazarotenic acid binds preferentially to RAR-β and RAR-γ (higher affinity for these than RAR-α; little to no meaningful RXR activity).
- The ligand-receptor complex forms heterodimers (usually with RXR), binds retinoic acid response elements (RAREs) on DNA, and regulates gene transcription.
- Also antagonizes AP-1 (c-Jun/c-Fos) signaling, reducing inflammation and matrix metalloproteinase activity.
Downstream effects:
- Normalizes keratinocyte differentiation and proliferation > reduces hyperkeratosis and comedone formation (comedolytic).
- Anti-inflammatory > downregulates inflammatory markers.
- Induces specific genes: Tazarotene induced genes (TIG1, TIG2, TIG3), which have antiproliferative effects.
- In psoriasis: Reduces hyperproliferative keratins (K6, K16), transglutaminase, involucrin, and other markers of abnormal differentiation and inflammation.
- In acne: Decreases microcomedones, reduces inflammatory lesions, and helps prevent new ones.
- Some collagen-modulating and anti-photoaging effects via gene regulation and AP-1 inhibition.
Because it is more selective (especially for RAR-β/γ, which are abundant in epidermis), it can be more potent than tretinoin in some studies but often more irritating.
3. Approved Uses and Efficacy
| Condition | Strength of Evidence | Typical Results |
|---|---|---|
| Acne vulgaris (mild to severe) | Strong | Reduces both inflammatory and non-inflammatory lesions; often slightly more effective than tretinoin or adapalene in head-to-head trials |
| Plaque psoriasis (stable, limited BSA) | Strong | Improves plaque elevation, scaling, and erythema; can have residual benefit after stopping |
| Photoaging / fine wrinkles / mottled hyperpigmentation | Moderate (Avage) | Improves fine lines, texture, and dyspigmentation with continued use |
It is sometimes used off-label for other keratinization disorders or as part of combination regimens (e.g., with topical corticosteroids for psoriasis).
4. Dosing and Application
- Acne: Usually 0.1% (cream, gel, or foam) or 0.045% lotion once daily in the evening to affected areas.
- Psoriasis: Start with 0.05% once daily in the evening on plaques only; increase to 0.1% if tolerated and needed. Limit to ≤20% body surface area for gel in some labels.
- Photoaging: 0.1% cream once daily in the evening.
How to use:
- Apply a thin layer to clean, dry skin at night.
- Start slowly (every other night or buffered with moisturizer) to reduce irritation.
- Use a pea-sized amount for the face.
- Always use broad-spectrum sunscreen daily (increases photosensitivity).
- Moisturize liberally.
- Avoid eyes, mouth, and mucous membranes.
- Do not use on broken or eczematous skin.
5. Side Effects
Very common (local):
- Dryness, peeling/desquamation, redness (erythema), burning/stinging, itching, irritation.
These are usually dose- and vehicle-dependent and often improve after the first few weeks with proper moisturization and gradual introduction. Higher strengths (0.1%) cause more irritation than 0.05% or the 0.045% lotion.
Less common:
- Skin discoloration
- Increased sensitivity to sun or weather
Serious / important:
- Photosensitivity — strict sun protection required.
Systemic side effects are rare because absorption is low when used as directed on limited areas.
6. Comparison to Other Topical Retinoids
| Feature | Tazarotene | Tretinoin | Adapalene |
|---|---|---|---|
| Receptor selectivity | Preferential RAR-β/γ | Pan-RAR (α, β, γ) | Preferential RAR-β/γ |
| Potency for acne | Often slightly higher | High | High |
| Irritation | Usually highest | Moderate–high | Lowest |
| Psoriasis indication | Yes | No | No |
| Photoaging data | Good | Strongest/longest | Moderate (higher strengths) |
| Stability with benzoyl peroxide | Generally stable | Some formulations unstable | Stable |
| Pregnancy category | Contraindicated | Caution (C) | Caution (C) |
Tazarotene is often chosen when stronger efficacy is needed (especially for thicker lesions or psoriasis) and the patient can tolerate more irritation. Adapalene is usually preferred for sensitive skin. Tretinoin remains the most studied for anti-aging.
7. Practical Tips and Considerations
- Start low and slow — many people need a 2–4 week adjustment period.
- Combine with a good moisturizer (sandwich method if needed).
- For psoriasis, combining with a mid- or high-potency topical corticosteroid can improve results and reduce irritation.
- Avoid waxing, harsh scrubs, or other strong actives until tolerated.
- Results for acne usually appear in 4–12 weeks; psoriasis improvement can start in 1–4 weeks.
- Not for use in pregnancy or if trying to conceive.
- Keep away from eyes and apply only to affected areas when treating psoriasis.
Full Estriol Cream Guide
Thread Song 3
Estriol moved through the aging city of the Skin like a devoted lover. She did not demand or force. She arrived softly, settling into the tired places with quiet affection, reminding the cells of the care they once knew. Where thickness had faded and moisture had slipped away, she lingered close, offering steady warmth and gentle encouragement.
Night after night she returned, patient and attentive. She helped the deeper layers rebuild collagen, held water where it was needed, and restored a quiet firmness to what had grown thin. There was no harshness in her touch—only consistent, caring presence that allowed the Skin to soften, strengthen, and feel supported again.
In time the city stood fuller and more at ease, its surface smoother and its structure more resilient. Estriol, the lover, never sought to dominate. She simply gave what was missing, stayed long enough to make a difference, and left the Skin feeling quietly cherished and renewed.
Night after night she returned, patient and attentive. She helped the deeper layers rebuild collagen, held water where it was needed, and restored a quiet firmness to what had grown thin. There was no harshness in her touch—only consistent, caring presence that allowed the Skin to soften, strengthen, and feel supported again.
In time the city stood fuller and more at ease, its surface smoother and its structure more resilient. Estriol, the lover, never sought to dominate. She simply gave what was missing, stayed long enough to make a difference, and left the Skin feeling quietly cherished and renewed.
Topical estriol cream is a weak estrogen preparation sometimes used on the skin for its potential to support collagen, thickness, hydration, and firmness. Effects appear linked to estrogen receptor activation in skin cells. Evidence is promising but still limited, and individual response varies.
Estriol Cream for Skin – Full Guide
Estriol is a weak, naturally occurring estrogen. When used in cream form on the skin, it is mainly discussed for its potential anti-aging and skin-quality benefits, especially in people with lower estrogen levels. This guide focuses only on topical skin use.
Estriol (E3) is one of the three main human estrogens. It is the weakest of the three and binds estrogen receptors with lower affinity and for a shorter time than estradiol. Because of this milder activity, it is sometimes preferred in compounded topical creams intended for the skin.
Skin contains estrogen receptors (ERα and ERβ). When estriol binds these receptors in the epidermis and dermis, it can:
These effects are most relevant when natural estrogen levels have declined, as collagen and skin thickness naturally decrease in that setting.
Available studies (mostly small and in postmenopausal women) suggest topical estriol may help with:
Results are generally modest and develop gradually over weeks to months. Evidence is still limited compared with well-studied ingredients like retinoids or vitamin C.
Compounded estriol creams for facial or body skin commonly range from 0.01% to 0.3%.
General application approach (always follow your prescriber’s instructions):
Do not use large amounts or apply over large body areas unless specifically directed.
Possible local effects:
Systemic considerations:
Quality and exact concentration can vary with compounded products, so a reputable compounding pharmacy is important.
Estriol is a weak, naturally occurring estrogen. When used in cream form on the skin, it is mainly discussed for its potential anti-aging and skin-quality benefits, especially in people with lower estrogen levels. This guide focuses only on topical skin use.
1. What Is Estriol?
Estriol (E3) is one of the three main human estrogens. It is the weakest of the three and binds estrogen receptors with lower affinity and for a shorter time than estradiol. Because of this milder activity, it is sometimes preferred in compounded topical creams intended for the skin.
2. How It Works on Skin
Skin contains estrogen receptors (ERα and ERβ). When estriol binds these receptors in the epidermis and dermis, it can:
- Stimulate fibroblasts to increase production of collagen (especially types I and III)
- Support glycosaminoglycans (including hyaluronic acid) that help hold moisture
- Improve skin thickness and density
- Enhance hydration and barrier function
- Support elasticity and firmness
These effects are most relevant when natural estrogen levels have declined, as collagen and skin thickness naturally decrease in that setting.
3. Potential Skin Benefits
Available studies (mostly small and in postmenopausal women) suggest topical estriol may help with:
- Increased skin thickness and collagen content
- Improved firmness and elasticity
- Better hydration
- Reduction in the appearance of fine wrinkles
- Smoother texture
Results are generally modest and develop gradually over weeks to months. Evidence is still limited compared with well-studied ingredients like retinoids or vitamin C.
4. Typical Strengths and Application for Skin
Compounded estriol creams for facial or body skin commonly range from 0.01% to 0.3%.
General application approach (always follow your prescriber’s instructions):
- Start with a low strength and lower frequency (e.g., a few nights per week)
- Use a very small amount (pea sized or less for the face)
- Apply to clean skin, usually in the evening
- Follow with moisturizer if needed
- Use daily broad-spectrum sunscreen, as with most active skincare
Do not use large amounts or apply over large body areas unless specifically directed.
5. Side Effects and Safety Considerations
Possible local effects:
- Mild irritation, redness, or dryness (especially when starting)
- Temporary increase in sensitivity
Systemic considerations:
- Low strength topical use on limited areas (such as the face) typically produces minimal systemic absorption in available studies.
- People with a history of hormone-sensitive conditions should discuss use with their doctor.
- Not for use during pregnancy.
- Long-term safety data specifically for facial anti-aging use remain limited.
Quality and exact concentration can vary with compounded products, so a reputable compounding pharmacy is important.
6. Practical Tips
- Introduce slowly to assess tolerance.
- Pair with a solid basic routine (cleanser, moisturizer, sunscreen).
- Results, if any, are gradual — consistent use over several months is usually needed to judge benefit.
- It is not a replacement for proven actives such as retinoids, but some people use it alongside them under guidance.
- Regular check-ins with a knowledgeable healthcare provider are recommended.
My End Of Guide Notes
Lol this took a long ass time of revision and testing.
I had to find out how to format correctly which took me hours and a failed thread, https://looksmax.org/threads/clenbuterol-the-adventurer-full-clen-guide.2326657/(Literally posted this blank and had to completely paste it google docs again in under 30 minutes)
I finally got the formatting correct in this guide below though which was sort of a test for this thread
Ive been making and revising this for a bit of while now because skin shit is already talked about a lot but i decided to lock in on it and make it a story.
Everyone LOVES my story guides.
Anyway Hope You Enjoyed
(EDIT):THE POINT OF THE SOURCES WAS SO I CAN SHOW YOU WHERE I GOT THE INFORMATION. WHY IS HE SO STUPID.
I ALSO USE DASHES IN LOTS OF MY REGULAR THREADS TOO
(Edit 2) I removed all unnecessary symbols
SOURCES: For the Info (NOT FOR THE PRODUCTS)
Isotretinoin (oral route) - Side effects & dosage
www.mayoclinic.org
Tretinoin Cream: The Ultimate Guide | Academic Alliance in Dermatology
Tretinoin cream has become a cornerstone in many skincare routines, and for good reason. From acne to anti-aging, this wonder cream is a fan favorite.
www.academicallderm.com
Tretinoin: Complete Guide for Acne and Aging
How tretinoin works, available strengths, the realistic timeline, and how it compares to over-the-counter retinol.
pimpl.com
GHK-Cu Dosage and Protocol: A Medical Provider's Guide to the 30-Day Cycle
GHK-Cu dosage at Perfect B Doral FL: 1 mg/day days 1-15, 2 mg/day days 16-30, 30-day cycle. Protocol, reconstitution guide, and clinical outcomes.
www.perfectb.com
Tazarotene Induces Apoptosis in Human Basal Cell Carcinoma via Activation of Caspase-8/t-Bid and the Reactive Oxygen Species-Dependent Mitochondrial Pathway - PMC
Previous studies suggest that tazarotene, a new member of the acetylenic class of RARβ/γ selective retinoids which is approved to treat a variety of skin diseases, exhibits an anti-proliferative effect in human basal cell carcinoma (BCC) by ...
pmc.ncbi.nlm.nih.gov
@Stalker @Fynn @averagetotaluser @Volpa
#VolpaMogs
(Giveaways over but maybe i can win in spirit
)
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