Cartalax
What do these badges mean?
Evidence tier
- AHuman-validated — Human trials showing positive results and good safety.
- BAnimal-grade — No human trials yet, but solid animal/preclinical evidence of effect and safety.
- CAnecdotal — No human or animal trials — only anecdotal/observational reports.
- DInsufficient evidence — No or insufficient evidence (encyclopedia only — never recommended by the builder).
Safety light
- 🟢 Green — Only mild, manageable side effects; reasonable safety data.
- 🟡 Yellow — Needs active management, has a meaningful contraindication/interaction, or has thin long-term data.
- 🔴 Red — Risk of a hospital-level event — treat with serious caution.
Browse-only — not on the protocol builder's curated shortlist, so the builder won't recommend it.
What is it?
Cartalax is a Khavinson tripeptide (Ala-Glu-Asp) developed from cartilage tissue, claimed to target connective tissue cells and fibroblasts. The name suggests cartilage-specific action, but the published research is primarily on fibroblasts (the cells that build and maintain connective tissue broadly: cartilage, tendons, ligaments, skin, blood vessel walls) and kidney cells — not on cartilage tissue directly. The connective-tissue benefit is a mechanistic inference from the fibroblast work, not a proven cartilage outcome.
What does it do in my body?
Like all Khavinson short peptides, AED is proposed to enter the cell nucleus, bind DNA in the minor groove, and modulate gene expression in a tissue-specific way. For Cartalax, the published data characterizes this as epigenetic: the peptide shifts which genes aging fibroblasts and kidney cells are actively reading, pulling the pattern back toward a younger cell’s profile. Molecular docking simulations in Khavinson et al. 2014 model the AED–DNA minor-groove interaction underlying this claim.
How can it help me?
- Where the science stands: Emerging / in-vitro — 3 primary Khavinson-group papers (2 using human-derived cells), no animal-in-vivo or human data
The full evidence — every human, animal, and lab study, graded — is one tap away: use the See the deeper science → toggle at the top.
Is it dangerous? What are the side effects?
Well tolerated in community use — injection-site redness and transient swelling are the most commonly reported events. No serious AEs documented in Russian literature or community reports. Long-term human safety data does not exist.
Cancer / history of cancer = hard contraindication. The AED mechanism includes p53 suppression and enhanced cell proliferation — exactly the profile that warrants caution in active malignancy. Cartalax has never been studied in oncology patients. This is not a risk OHM softens; it’s a routing point to the patient’s oncologist.
The real risk isn’t only the molecule — it’s also the supply chain. Khavinson-family peptides are the dominant gray-market counterfeit category in the peptide space. Third-party COA verification matters more here than for almost any other peptide class.
Regulatory status: Cartalax is research_only in the US — not FDA-approved for human use, sold as a research compound, not eligible for compounding. It is not a controlled substance.
Part 1 — How to reconstitute it
What's used: bacteriostatic water (sterile, preserved water the powder is mixed with) and a separate, larger reconstitution syringe used only for mixing — not the small syringe used for administration.
No human dose-finding study exists for either range. Reconstitution (community protocol): 20 mg vial + 2 mL bacteriostatic water → 2 mg dose = 20 units on a U-100 insulin syringe; morning preferred.
How it's mixed
- The vial is tilted and the bacteriostatic water is added slowly down the inside glass wall — not squirted straight onto the powder.
- It is swirled gently to dissolve. It is never shaken — shaking can damage the peptide.
- The reconstituted vial is stored refrigerated and out of light.
- Reconstituted peptides are commonly used within a few weeks, inside the beyond-use window the source specifies — that window varies by peptide.
The free reconstitution calculator does the concentration math for any vial size and water volume, including the equivalent units on an insulin syringe.
Part 2 — Typical dosing
Educational context only — talk to a licensed medical provider before any protocol. What follows describes the doses and schedules most commonly reported in the research and by practitioners, shared so you can have an informed conversation. These compounds are sold for research use only, are not FDA-approved drugs, and this is not medical advice.
Administration as reported. Reported practice is subcutaneous administration (into the fat just under the skin) using a 0.3 mL U-100 insulin syringe, with sites rotated.
Educational purposes only — this reflects the Khavinson-school and community protocol conventions, stated plainly; it is not medical advice.
Dosing (community protocols — significant source discrepancy):
| Protocol source | Dose | Cycle | Notes |
|---|---|---|---|
| Khavinson-school (ASCEND, combination protocol) | 5–10 mcg/day | 10 days; 1–3× per year | Very low; may reflect a multi-peptide combination protocol where total bioregulator load is distributed across peptides |
| Community consensus (Holyfield 2026, general community) | 2 mg/day | 10–20 days; 3–4× per year | 200–400× higher than Khavinson-school dose; no dose-finding study to adjudicate |
This shares the broader Khavinson-family cycle shape — short pulse, spaced rest, repeated a few times a year — but Cartalax is the clearest case in the whole family of two dosing conventions that don’t just differ, they diverge by two to three orders of magnitude, with nothing to say which is right.
What should I avoid combining — and what's synergistic?
Cartalax doesn't have a dedicated stacking protocol in our notes — the interactions that matter most are in the safety section above. For how people combine it with other peptides, the deeper-science view has the full detail.
Where do people source this?
OHM does not sell or handle any compound. Research-use-only material is sold by third-party vendors; our vetting notes and disclosures are on the Where to buy page. If you'd rather have a physician in the loop, see the telehealth option. Whatever the route, the supply chain is the real risk: only consider vendors that publish batch-level third-party Certificates of Analysis.
Cartalax (Ala-Glu-Asp / AED) is a Khavinson tripeptide developed from cartilage tissue, targeting connective-tissue cells and fibroblasts. It’s a maintenance and longevity compound, not an acute repair tool — for active joint injury, BPC-157 and TB-500 have a far stronger evidence base. Three in-vitro papers anchor real, if preclinical-only, evidence; the community dosing convention and the Khavinson-school dosing convention disagree by 200–400×, and no dose-finding study exists to adjudicate.
| Class | Khavinson tripeptide — Ala-Glu-Asp (AED), developed from cartilage tissue |
| Mechanism (one line) | Proposed to bind DNA in the minor groove and shift gene expression in aging fibroblasts and kidney cells toward a younger profile |
| Evidence base | Emerging / in-vitro — 3 primary Khavinson-group papers (2 using human-derived cells), no animal-in-vivo or human data |
| Safety record | Well tolerated in community use (injection-site redness/swelling); hard contraindication in active or historical cancer |
| Regulatory status | research_only in the US, not FDA-approved |
What it is
Cartalax is a Khavinson tripeptide (Ala-Glu-Asp) developed from cartilage tissue, claimed to target connective tissue cells and fibroblasts. The name suggests cartilage-specific action, but the published research is primarily on fibroblasts (the cells that build and maintain connective tissue broadly: cartilage, tendons, ligaments, skin, blood vessel walls) and kidney cells — not on cartilage tissue directly. The connective-tissue benefit is a mechanistic inference from the fibroblast work, not a proven cartilage outcome.
How it works
Like all Khavinson short peptides, AED is proposed to enter the cell nucleus, bind DNA in the minor groove, and modulate gene expression in a tissue-specific way. For Cartalax, the published data characterizes this as epigenetic: the peptide shifts which genes aging fibroblasts and kidney cells are actively reading, pulling the pattern back toward a younger cell’s profile. Molecular docking simulations in Khavinson et al. 2014 model the AED–DNA minor-groove interaction underlying this claim.
What the research shows
Skin fibroblast studies (the primary evidence base):
- Linkova NS et al. 2016. “Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro.” Bull Exp Biol Med 161:175-178. DOI: 10.1007/s10517-016-3370-x · 27259496 — AED peptide in a rat skin fibroblast replicative-aging model. Key outcomes: regulated synthesis of Ki-67 (proliferation marker), CD98hc (glycoprotein), Caspase-3, and MMP-9. MMP-9 inhibition is the commercially relevant finding: matrix metalloproteinase 9 breaks down structural ECM components (collagen, fibronectin) and ramps up with age; AED appears to suppress it.
- Fridman NV, Linkova NS, Khavinson VKh et al. 2020. “Comparison of the Effects of KE and AED Peptides on Functional Activity of Human Skin Fibroblasts during Their Replicative Aging.” Bull Exp Biol Med 170(1):154-157. 33231794 — AED in human skin fibroblasts (higher confidence than rat-derived cells): activated synthesis of SIRT-1 and SIRT-6; stimulated collagen I synthesis. Geroprotective effect confirmed in human-derived cells. SIRT-1 and SIRT-6 are NAD±dependent deacylases central to genome maintenance, metabolic regulation, and longevity pathways.
Kidney cell study (anti-senescence mechanism):
-
Khavinson VKh, Tarnovskaia SI, Linkova NS et al. 2014. “Tripeptides slow down aging process in renal cell culture.” Adv Gerontol 27(4):651-6. 25946838 — AED (+ EDL tripeptide) in rat kidney cell culture: increased cell proliferation; decreased p16, p21, p53 (pro-senescence markers); increased SIRT-6 expression. Molecular docking in the same paper models the AED–DNA minor-groove interaction underlying the epigenetic mechanism.
The anti-senescence picture in plain terms: p16 (CDKN2A) and p21 (CDKN1A) are CDK inhibitors that push cells into senescence when activated — their suppression keeps cells in an active, proliferating state. SIRT-6 upregulation is the longevity co-signal: SIRT-6 regulates DNA double-strand-break repair, telomere stability, and NF-κB–driven inflammation; its decline with age is a driver of multiple aging phenotypes. Importantly, p53 suppression is also noted — p53 is a master regulator of senescence and apoptosis, though its suppression in a cancer context is a concern (see cancer contraindication below).
Review mention:
- Khavinson VKh 2020. “[Short peptides: regulation of skin function during aging]” · 32362083
[REVIEW]— names AED as one of the “polyfunctional peptides” that slow apoptosis, stimulate skin cell proliferation, increase fibroblast functional activity, and normalize intracellular matrix hemostasis. Lists AED alongside AEDG (Epithalon) and KED (Vilon) as separate compounds — important confirmation that AED ≠ AEDG.
The honest evidence read. Three in-vitro papers from the Khavinson group, all preclinical, no independent Western replication, no animal-in-vivo or human data. This is the standard Khavinson-family limitation — the research is internally consistent and the lab signals are real, but the clinical question is entirely open. An upgrade from 0-cited to emerging-in-vitro is warranted; a D/provisional grade is still correct.
Positioning vs BPC-157 and TB-500. Cartalax is a maintenance and longevity compound, not an acute repair tool. For active joint injury, BPC-157 and TB-500 have a far stronger evidence base and clinical track record — they’re the right call by a wide margin. Cartalax makes sense as a long-term add-on once the acute picture is handled: connective-tissue upkeep, cellular age-related decline in fibroblast function, longevity framing. Foundations first (training, protein, sleep, load management) — Cartalax is a reasoned add-on at that level, not a substitute for any of them.
Real-world protocol
Educational purposes only — this reflects the Khavinson-school and community protocol conventions, stated plainly; it is not medical advice.
Dosing (community protocols — significant source discrepancy):
| Protocol source | Dose | Cycle | Notes |
|---|---|---|---|
| Khavinson-school (ASCEND, combination protocol) | 5–10 mcg/day | 10 days; 1–3× per year | Very low; may reflect a multi-peptide combination protocol where total bioregulator load is distributed across peptides |
| Community consensus (Holyfield 2026, general community) | 2 mg/day | 10–20 days; 3–4× per year | 200–400× higher than Khavinson-school dose; no dose-finding study to adjudicate |
No human dose-finding study exists for either range. Reconstitution (community protocol): 20 mg vial + 2 mL bacteriostatic water → 2 mg dose = 20 units on a U-100 insulin syringe; morning preferred.
This shares the broader Khavinson-family cycle shape — short pulse, spaced rest, repeated a few times a year — but Cartalax is the clearest case in the whole family of two dosing conventions that don’t just differ, they diverge by two to three orders of magnitude, with nothing to say which is right.
Side effects & management
Well tolerated in community use — injection-site redness and transient swelling are the most commonly reported events. No serious AEs documented in Russian literature or community reports. Long-term human safety data does not exist.
Cancer / history of cancer = hard contraindication. The AED mechanism includes p53 suppression and enhanced cell proliferation — exactly the profile that warrants caution in active malignancy. Cartalax has never been studied in oncology patients. This is not a risk OHM softens; it’s a routing point to the patient’s oncologist.
The real risk isn’t only the molecule — it’s also the supply chain. Khavinson-family peptides are the dominant gray-market counterfeit category in the peptide space. Third-party COA verification matters more here than for almost any other peptide class.
Regulatory status
Cartalax is research_only in the US — not FDA-approved for human use, sold as a research compound, not eligible for compounding. It is not a controlled substance.
Sources
- primary profile (thepeptidelist.com directory capture, 2026-06-07).
- Josh Holyfield YouTube digest (2026-07-13). Primary source for the mechanism expansion, MMP-9 fibroblast data, kidney-cell anti-senescence framing, community dosing protocol, and positioning vs BPC-157/TB-500. Triggered the verification pass that resolved the sequence error (AED not AEDG) and confirmed PMIDs 27259496, 33231794, 25946838, 32362083.
- 0035 tier/safety/goal grading: Cartalax kept D-provisional / encyclopedia-only, upheld after the evidence upgrade.
- PMIDs: 27259496 (Linkova et al. 2016), 33231794 (Fridman/Linkova/Khavinson 2020), 25946838 (Khavinson/Tarnovskaia/Linkova 2014), 32362083 (Khavinson 2020 review)/
[REVIEW]. - Related: BPC-157 · TB-500 · Wolverine (BPC-157 + TB-500) · GHK-Cu · GLOW · Epithalon · Vilon · the Khavinson bioregulator family.
Sources & references
- primary profile (thepeptidelist.com directory capture, 2026-06-07).
- Josh Holyfield YouTube digest (2026-07-13). Primary source for the mechanism expansion, MMP-9 fibroblast data, kidney-cell anti-senescence framing, community dosing protocol, and positioning vs BPC-157/TB-500. Triggered the verification pass that resolved the sequence error (AED not AEDG) and confirmed PMIDs 27259496, 33231794, 25946838, 32362083.
- 0035 tier/safety/goal grading: Cartalax kept D-provisional / encyclopedia-only, upheld after the evidence upgrade.
- PMIDs: 27259496 (Linkova et al. 2016), 33231794 (Fridman/Linkova/Khavinson 2020), 25946838 (Khavinson/Tarnovskaia/Linkova 2014), 32362083 (Khavinson 2020 review)/
[REVIEW]. - Related: BPC-157 · TB-500 · Wolverine (BPC-157 + TB-500) · GHK-Cu · GLOW · Epithalon · Vilon · the Khavinson bioregulator family.