Cat's Claw for Rheumatoid Arthritis

Rheumatoid arthritis is the highest-quality clinical evidence base for Cat's Claw in any indication. The Mur 2002 randomized double-blind placebo-controlled trial of pentacyclic-alkaloid-standardized Uncaria tomentosa extract added to background DMARD therapy (sulfasalazine or hydroxychloroquine) in 40 RA patients showed a 53% reduction in the number of painful joints and a 43% reduction in the number of swollen joints at week 24, against a placebo arm that had no significant change. The Piscoya 2001 trial of freeze-dried Uncaria guianensis in osteoarthritis of the knee showed comparable benefit on knee pain at four weeks. The mechanism is upstream NF-kB inhibition with downstream TNF-alpha suppression — the same pathway targeted by methotrexate, sulfasalazine, and biologics like adalimumab, but reached pharmacologically rather than through immune-cell-targeting drugs. Critical positioning: Cat's Claw is an adjunct to, never a substitute for, conventional RA disease-modifying therapy. Untreated RA destroys joint architecture in the first two years — the window during which DMARDs and biologics produce the largest long-term outcome benefit. Cat's Claw added on top can reduce symptoms and possibly reduce required DMARD dose, but starting Cat's Claw and refusing methotrexate is a path to joint destruction.

Rheumatoid Arthritis — What Cat's Claw Is and Isn't For
The Mur 2002 24-Week RCT in Detail
The Piscoya 2001 Osteoarthritis Trial
The NF-kB / TNF-alpha Mechanism
Cat's Claw vs DMARDs (Methotrexate, Sulfasalazine, Hydroxychloroquine)
Cat's Claw vs Biologics (TNF Inhibitors, IL-6 Inhibitors)
Cat's Claw vs NSAIDs and Steroids
Why Chemotype Determines Whether the Trial Reproduces
Practical Adjunctive Protocol
Cautions and When to Avoid
Key Research Papers
Connections

Rheumatoid Arthritis — What Cat's Claw Is and Isn't For

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which the immune system attacks the synovial lining of joints, producing chronic inflammation, pain, swelling, eventual cartilage destruction, bone erosion, and joint deformity. It typically presents symmetrically in the small joints of the hands and feet, often progressing to involve wrists, elbows, knees, shoulders, and cervical spine. Disease activity is measured clinically (tender joint count, swollen joint count, patient global assessment), serologically (rheumatoid factor, anti-CCP antibodies, ESR, CRP), and increasingly by joint imaging (ultrasound or MRI showing synovitis or erosions).

The most consequential clinical fact about RA is the "window of opportunity" concept: the first one to two years after symptom onset is the period during which joint architecture can be preserved if disease-modifying therapy is initiated promptly. Once cartilage is destroyed and bony erosions appear on imaging, they do not heal even if subsequent inflammation is controlled. Modern rheumatology therefore aggressively initiates conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs — methotrexate first-line, sulfasalazine or hydroxychloroquine as alternatives or adjuncts) within weeks to months of diagnosis, with escalation to biologic DMARDs (TNF inhibitors, IL-6 inhibitors, JAK inhibitors, anti-CD20) if disease remains active.

This is the context in which Cat's Claw should be understood. Cat's Claw is an adjunctive symptom-control and inflammation-reduction agent, used on top of conventional DMARD therapy. It is not a disease-modifying agent in the sense that methotrexate is — there is no evidence it prevents radiographic joint erosion or alters long-term disability outcomes. Patients who choose Cat's Claw instead of DMARDs in the early-disease window risk permanent joint destruction during the years they spend with uncontrolled inflammation.

The legitimate role of Cat's Claw in RA, supported by the Mur trial, is as an add-on to a stable DMARD regimen for patients with residual symptomatic activity. In that role, the evidence is real and the safety profile is favorable.

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The Mur 2002 24-Week RCT in Detail

The Mur, Hartig, Eibl, and Schirmer trial published in the Journal of Rheumatology in 2002 is the foundational clinical evidence for Cat's Claw in rheumatoid arthritis. The trial was conducted at the Department of Internal Medicine, University of Innsbruck, Austria — Klaus Keplinger's home institution and the European center of Cat's Claw clinical research.

Design. Randomized, double-blind, placebo-controlled, 24-week parallel-arm trial. 40 patients with active rheumatoid arthritis who had been on stable background DMARD therapy (sulfasalazine or hydroxychloroquine) for at least six months. Randomization was 1:1 to Cat's Claw extract or matching placebo.

Intervention. The active extract was a pentacyclic-alkaloid-chemotype standardized preparation of Uncaria tomentosa bark, dosed at 60 mg of the standardized extract per day for the first 24 weeks. The extract was selected and verified to contain pentacyclic oxindole alkaloids with negligible tetracyclic alkaloid contamination — the critical chemotype distinction that determines whether Cat's Claw immune modulation occurs at all (see Immune Modulation deep-dive).

Background therapy. All patients continued their existing DMARD therapy and were permitted stable doses of NSAIDs and low-dose oral prednisone (under 10 mg/day) throughout the trial. Dose changes were not permitted during the study period.

Outcome measures. Primary outcomes were number of painful joints and number of swollen joints. Secondary outcomes included Ritchie articular index, duration of morning stiffness, patient and physician global assessments, and laboratory inflammation markers (ESR, CRP).

Results at 24 weeks.

Number of painful joints reduced by 53% in the Cat's Claw group; no significant change in the placebo group. The between-group difference was statistically significant.
Number of swollen joints reduced by 43% in the Cat's Claw group; no significant change in the placebo group.
Ritchie articular index showed similar pattern of significant improvement only in the Cat's Claw group.
Patient global assessment improved significantly in the Cat's Claw group.
ESR and CRP showed modest reduction in the Cat's Claw group but the change did not reach statistical significance — consistent with a clinical effect that may slightly outpace the laboratory marker change in early-term studies.
No serious adverse events were reported in either arm. Mild gastrointestinal complaints occurred at similar rates in both groups.

Phase 2 (weeks 24–52, open-label extension). After week 24, all patients in the trial — both original Cat's Claw recipients and original placebo recipients — received open-label Cat's Claw extract for an additional 28 weeks. The original Cat's Claw group maintained their improvement. The originally placebo group, who had not improved in the blinded phase, showed significant reduction in painful joints during the open-label phase, providing within-subject confirmation of the Cat's Claw effect.

Limitations to note. The trial was small (40 patients) and the dose (60 mg/day standardized extract) is low compared to many retail Cat's Claw products. The selected DMARDs (sulfasalazine, hydroxychloroquine) are weaker DMARDs than methotrexate, which is the modern first-line choice — results may differ in a methotrexate-background population. The trial did not include radiographic outcomes, so the question of whether Cat's Claw modifies joint structural progression remains unanswered. Replication in a larger trial with methotrexate background, including imaging endpoints, would strengthen the evidence substantially but has not been done in the 20+ years since publication.

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The Piscoya 2001 Osteoarthritis Trial

The Piscoya, Rodriguez, Bustamante et al. trial published in Inflammation Research in 2001 examined freeze-dried Uncaria guianensis (the related species, not U. tomentosa) in osteoarthritis of the knee. The choice of species matters: U. guianensis has its own anti-inflammatory profile that overlaps with but is not identical to U. tomentosa.

Design. Randomized, double-blind, placebo-controlled, 4-week trial. 45 patients with osteoarthritis of the knee diagnosed by clinical and radiographic criteria. Randomization was 2:1 to active extract or placebo.

Intervention. Freeze-dried Uncaria guianensis bark, 100 mg/day for 4 weeks.

Results.

Pain associated with activity was significantly reduced in the Cat's Claw group within the first week and continued to improve over the trial.
Pain at rest and pain at night were not significantly different between groups, suggesting the effect was strongest in the inflammatory-loaded state.
Knee circumference did not change, indicating the symptomatic improvement was not driven by gross reduction in effusion.
No significant adverse events.

Mechanistic correlative work in the same study examined the effect of the extract on ex-vivo TNF-alpha and prostaglandin E2 production by activated macrophages. The extract significantly suppressed TNF-alpha production at concentrations achievable through oral dosing but had minimal effect on prostaglandin E2 — an interesting pattern suggesting Cat's Claw acts upstream of the COX pathway and primarily through cytokine modulation rather than through prostaglandin inhibition (the NSAID mechanism).

The Piscoya trial is shorter and smaller than the Mur trial, and used U. guianensis rather than U. tomentosa, so the two studies should be considered separately. But the directionality is consistent with the broader Cat's Claw inflammation-modulating story.

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The NF-kB / TNF-alpha Mechanism

The mechanistic story behind Cat's Claw in arthritis is straightforward and well-mapped to the modern understanding of RA pathogenesis. Nuclear factor kappa-B (NF-kB) is a transcription factor complex that sits inactive in the cytoplasm of resting cells, sequestered by its inhibitor protein IkB. When activating signals reach the cell (TNF-alpha binding to TNFR1, IL-1 binding to IL-1R, bacterial lipopolysaccharide binding to TLR4, and many others), the IkB inhibitor is phosphorylated and degraded, releasing NF-kB to translocate into the nucleus and bind to specific DNA sequences (NF-kB response elements) in the promoter regions of inflammatory target genes.

The downstream gene products driven by NF-kB activation include:

Cytokines: TNF-alpha (creating a positive feedback loop), IL-1, IL-6, IL-8
Adhesion molecules: ICAM-1, VCAM-1, E-selectin, recruiting more leukocytes to the inflammatory site
Enzymes: COX-2, iNOS, matrix metalloproteinases (which destroy cartilage)
Anti-apoptotic proteins: Bcl-2 family, prolonging the survival of inflammatory cells

In rheumatoid arthritis, persistent NF-kB activation in synovial macrophages, fibroblast-like synoviocytes, and infiltrating T cells is the molecular engine of chronic joint inflammation. The TNF-alpha output sustains the inflammatory loop, the matrix metalloproteinases destroy cartilage, and the anti-apoptotic gene products prevent the inflammatory cells from dying off on schedule.

Cat's Claw POA extracts inhibit NF-kB activation by approximately 65–85% at therapeutic concentrations — one of the most potent botanical NF-kB inhibitors documented. This was established by the Sandoval-Chacon group in 1998 (the foundational paper) and replicated by multiple subsequent investigators. The downstream consequence is reduced TNF-alpha output, reduced IL-1 and IL-6, reduced adhesion molecule expression, reduced matrix metalloproteinase, and reduced anti-apoptotic gene expression — the entire inflammatory cascade is dampened simultaneously rather than blocked at any single downstream effector.

This pleiotropic mechanism is one reason Cat's Claw produces clinical effects across multiple inflammatory conditions (rheumatoid arthritis, osteoarthritis, Crohn's-style colitis) at the same dose. It is also why head-to-head comparison with single-mechanism drugs (a TNF inhibitor, a COX-2 inhibitor) tends to favor the targeted drug at the level of any single cytokine endpoint while Cat's Claw produces broader, milder modulation across the full inflammatory cascade.

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Cat's Claw vs DMARDs (Methotrexate, Sulfasalazine, Hydroxychloroquine)

This is the most important comparison for any RA patient considering Cat's Claw.

Methotrexate is the modern first-line DMARD for rheumatoid arthritis. It is a folate antagonist that suppresses lymphocyte proliferation, downregulates pro-inflammatory cytokines, and has been shown in long-term trials to slow radiographic joint erosion. Typical dosing is 7.5–25 mg once weekly, with folic acid supplementation 1 mg/day to mitigate side effects. Methotrexate is unquestionably more powerful than Cat's Claw for disease control, and unquestionably has a real side-effect profile (hepatic toxicity, hematologic toxicity, oral ulcers, GI upset, teratogenicity). Cat's Claw is not a substitute for methotrexate in patients who tolerate it. Cat's Claw can reasonably be added to methotrexate as an adjunct in patients with residual symptoms — the mechanism of action is non-overlapping (NF-kB vs antiproliferative) so additive effect is plausible. There are no documented adverse interactions between methotrexate and Cat's Claw, but practitioner supervision is recommended.
Sulfasalazine is a sulfa-containing DMARD that is partly metabolized in the gut to sulfapyridine and 5-aminosalicylic acid. It is a moderate DMARD, often used in combination with methotrexate or hydroxychloroquine, with side effects including sulfa allergy reactions, hematologic toxicity, hepatic toxicity, GI upset, and male reversible oligospermia. The Mur trial used sulfasalazine and hydroxychloroquine as background DMARDs — the Cat's Claw effect was demonstrated in that specific combination. Cat's Claw may share part of the mechanism (anti-inflammatory at the gut level for sulfasalazine, NF-kB modulation for Cat's Claw) but the two are distinct molecules with different organ-level effects.
Hydroxychloroquine is a weaker DMARD originally developed as an antimalarial. It has anti-inflammatory and mild immunomodulatory effects via inhibition of lysosomal function in immune cells. It is well-tolerated long-term but has a rare cumulative retinal toxicity that requires annual ophthalmologic monitoring. Hydroxychloroquine and Cat's Claw share no overlapping mechanism, and combination use (as in the Mur trial) is reasonable.
Leflunomide, azathioprine, and JAK inhibitors (tofacitinib, baricitinib, upadacitinib) are additional csDMARDs and small-molecule DMARDs. Cat's Claw has not been studied in combination with any of these, and the immune-modulating overlap with JAK inhibitors specifically warrants practitioner supervision if combined use is considered.

The bottom-line clinical positioning: Cat's Claw is an adjunct, not a substitute. RA patients should be on appropriate conventional DMARD therapy as managed by a rheumatologist, with Cat's Claw considered as add-on therapy for residual symptoms or as a means of potentially reducing required NSAID or low-dose steroid burden.

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Cat's Claw vs Biologics (TNF Inhibitors, IL-6 Inhibitors)

Biologic DMARDs are large-molecule drugs that directly target specific cytokines or immune-cell surface markers. The major classes used in RA include TNF inhibitors (adalimumab, etanercept, infliximab, golimumab, certolizumab), IL-6 inhibitors (tocilizumab, sarilumab), IL-1 inhibitors (anakinra), anti-CD20 (rituximab), and anti-CD80/86 (abatacept). Biologics are typically reserved for patients with active disease despite csDMARD therapy. They are highly effective but expensive (often $20,000–$60,000/year retail in the US) and carry serious infection risk because they directly suppress key immune defenses.

Cat's Claw and biologics have mechanistic overlap — both reduce TNF-alpha activity — but operate at different levels and at vastly different magnitudes. A TNF inhibitor like adalimumab can bind and neutralize circulating TNF-alpha to near-zero levels; Cat's Claw modestly reduces TNF-alpha production via upstream NF-kB inhibition. The magnitudes are not comparable.

Combining Cat's Claw with biologics warrants particular caution. Theoretical concerns include:

Additive infection risk — biologics already increase risk of serious bacterial infections, tuberculosis reactivation, opportunistic fungal infections, and hepatitis B reactivation. Cat's Claw's broad immune-modulating profile makes the net direction on infection risk uncertain.
Unknown drug interactions — no formal pharmacokinetic or pharmacodynamic studies have been done.
Disease-flare risk on withdrawal — if Cat's Claw is contributing to control and is suddenly stopped, the patient may experience a disease flare.

The reasonable position: RA patients on biologics should not start Cat's Claw without explicit consultation with their rheumatologist. The clinical data to support combination use are essentially absent.

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Cat's Claw vs NSAIDs and Steroids

NSAIDs (ibuprofen, naproxen, diclofenac, meloxicam, celecoxib) are the symptomatic mainstay of arthritis pain control. They work through COX inhibition, blocking the conversion of arachidonic acid to inflammatory prostaglandins. They are effective for pain but do not modify disease progression in RA. Chronic NSAID use carries documented risks of gastric ulceration, kidney injury (especially in patients with reduced baseline kidney function or dehydration), and cardiovascular events (the COX-2 cardiovascular signal generalizes partially to non-selective NSAIDs).

Cat's Claw acts upstream of the COX pathway. In the Piscoya OA trial, Cat's Claw reduced TNF-alpha and clinical pain without significantly altering prostaglandin E2 production — suggesting the effect is genuinely through cytokine modulation rather than through prostaglandin inhibition. This is mechanistically attractive because it offers an anti-inflammatory effect with a different side-effect profile than NSAIDs.

The practical use case: patients with RA who are on conventional DMARD therapy but use chronic NSAIDs for symptom control may be able to reduce their NSAID burden by adding Cat's Claw. This is particularly attractive for patients with risk factors for NSAID side effects (older patients, those with reduced kidney function, those with history of gastric ulcer, those on anticoagulants). Dose reduction or discontinuation should be done in conversation with the prescribing physician, with assessment of disease activity before and after the change.

Low-dose oral prednisone (under 10 mg/day) is used in some RA patients as a bridge therapy while DMARDs reach full effect or in patients with breakthrough disease activity. Long-term low-dose steroids carry documented risks of osteoporosis, glucose intolerance, weight gain, skin thinning, and adrenal suppression. The Mur trial allowed continuation of stable low-dose prednisone, and Cat's Claw demonstrated benefit on top of that background. Whether Cat's Claw can substitute for low-dose steroids in well-controlled disease has not been specifically studied but is a reasonable adjunctive goal under rheumatologist supervision.

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Why Chemotype Determines Whether the Trial Reproduces

The Mur trial used a pentacyclic-alkaloid-standardized extract from a single batch with verified TOA contamination below 0.5%. The clinical effect observed in that trial cannot be expected from a TOA-contaminated bark powder, and the apparent failure of some RA patients to respond to retail "Cat's Claw" capsules may be a chemotype-quality problem rather than a real lack of effect.

This is the same chemotype story discussed at length in the Immune Modulation deep-dive and in the Benefits hub overview: 1% TOA contamination reduces POA immune activity by ~30%, and 10% TOA can reduce it by 70%+. Wild-harvested bark is a coin-flip on chemotype. Only laboratory-certified POA-standardized or TOA-free products can be expected to reproduce the Mur trial result.

For RA patients specifically, the practical choice is: Saventaro (the Austrian Keplinger preparation used in the trial environment, available in some European markets), C-Med-100 / AC-11 (the well-validated American preparation, available retail in the US), Samento (the TOA-free preparation, well-known from the Cowden Lyme protocol), or any other product whose label explicitly states POA standardization or TOA-free certification and lists alkaloid percentages in the certificate of analysis. A bottle from a generic supplement company that lists only "Cat's Claw bark 500 mg" with no chemotype data should be assumed to have unknown clinical activity.

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Practical Adjunctive Protocol

For a patient with rheumatoid arthritis on stable DMARD therapy (methotrexate, with or without sulfasalazine or hydroxychloroquine) who has residual symptomatic disease activity, the following adjunctive protocol approximates the Mur trial:

Product selection. A POA-standardized extract or C-Med-100. The Mur trial used 60 mg/day of pentacyclic-alkaloid-standardized extract. C-Med-100 is typically dosed at 350 mg/day (different standardization basis — the water-soluble fraction rather than alkaloid content).
Trial period. 24 weeks of consistent daily dosing before judging effect. Cat's Claw is not a fast-acting therapy; the Mur trial primary endpoint was at week 24.
Outcome tracking. Tender joint count, swollen joint count, morning stiffness duration in minutes, and patient global assessment (0–10 visual analog scale) at baseline and monthly. Standard RA lab markers (ESR, CRP, possibly DAS28 or CDAI composite scores) at baseline and at week 12 and week 24.
Communication with the rheumatologist. The rheumatologist should know that Cat's Claw is being added so that any change in disease activity is interpreted correctly and so that any decisions about DMARD dose changes account for the adjunctive therapy.
Stop criteria. Disease flare during the trial, evidence of allergic reaction, significant GI intolerance, or any signal of interaction with concurrent medication.
Continuation if successful. If symptomatic improvement is achieved, consider whether the rheumatologist would support a trial of NSAID or low-dose steroid dose reduction. The Mur extension data show benefit maintained out to 52 weeks; longer-term use is reasonable with periodic re-evaluation.

For RA patients on biologics (adalimumab, etanercept, infliximab, tocilizumab, etc.) — do not start Cat's Claw without explicit rheumatologist consultation. The combination has not been studied and the theoretical interaction concerns (additive infection risk, unknown PK/PD effects) warrant individualized risk assessment.

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Cautions and When to Avoid

Untreated active RA without conventional therapy — do not substitute. Patients within the first two years of symptom onset who choose Cat's Claw instead of conventional DMARD therapy risk permanent joint destruction. Cat's Claw is an adjunct, not a substitute.
Lupus, multiple sclerosis, and other autoimmune diseases — case-by-case. Unlike RA, where the NF-kB modulation favors symptom reduction, some autoimmune diseases may worsen with Cat's Claw's broader immune activation. The decision should be made with a rheumatologist or other specialist familiar with the specific disease and with Cat's Claw pharmacology.
Organ transplant on immunosuppressants — STRICT CONTRAINDICATION. Cat's Claw can counteract tacrolimus, cyclosporine, sirolimus, and mycophenolate, with potential for graft rejection. Avoid completely.
Pregnancy — CONTRAINDICATED. Traditional abortifacient use makes this a precautionary contraindication. RA patients planning pregnancy face a separate set of DMARD-management decisions that should be handled by the rheumatologist.
Methotrexate-treated patients planning pregnancy — methotrexate is itself teratogenic and must be discontinued months before conception. Cat's Claw is also contraindicated. Pregnancy in RA requires structured medication planning with the rheumatology team.
Hematologic abnormalities. Patients with platelet disorders, on anticoagulant therapy (warfarin, apixaban, rivaroxaban), or with planned surgery within 2–3 weeks should avoid Cat's Claw due to mild antiplatelet effects.
Allergic reactions. Cat's Claw is in the Rubiaceae family. Patients with known plant-family allergies should test cautiously. Discontinue if rash, swelling, or other hypersensitivity signs appear.
GI intolerance. The most common side effect is mild GI upset (nausea, soft stools, abdominal discomfort), usually resolving with dose reduction or with-food dosing.

For the broader anti-inflammatory and gastrointestinal applications and additional safety detail, see the anti-inflammatory deep-dive.

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Key Research Papers

Mur E, Hartig F, Eibl G, Schirmer M (2002). Randomized double blind trial of an extract from the pentacyclic alkaloid-chemotype of Uncaria tomentosa for the treatment of rheumatoid arthritis. Journal of Rheumatology 29(4): 678–681. — PubMed: Mur 2002 RA RCT
Piscoya J, Rodriguez Z, Bustamante SA, et al. (2001). Efficacy and safety of freeze-dried cat's claw in osteoarthritis of the knee: mechanisms of action of the species Uncaria guianensis. Inflammation Research 50(9): 442–448. — PubMed: Piscoya OA knee 2001
Sandoval-Chacon M, Thompson JH, Zhang XJ, et al. (1998). Antiinflammatory actions of cat's claw: the role of NF-kappaB. Alimentary Pharmacology & Therapeutics 12(12): 1279–1289. — PubMed: Sandoval-Chacon NF-kB 1998
Sandoval M, Charbonnet RM, Okuhama NN, et al. (2000). Cat's claw inhibits TNF-alpha production and scavenges free radicals: role in cytoprotection. Free Radical Biology and Medicine 29(1): 71–78. — PubMed: Sandoval TNF-alpha 2000
Sandoval M, Okuhama NN, Zhang XJ, et al. (2002). Anti-inflammatory and antioxidant activities of cat's claw (Uncaria tomentosa and Uncaria guianensis) are independent of their alkaloid content. Phytomedicine 9(4): 325–337. — PubMed: Sandoval alkaloid-independent 2002
Aguilar JL, Rojas P, Marcelo A, et al. (2002). Anti-inflammatory activity of two different extracts of Uncaria tomentosa. Journal of Ethnopharmacology 81(2): 271–276. — PubMed: Aguilar 2002
Keplinger K, Laus G, Wurm M, Dierich MP, Teppner H (1999). Uncaria tomentosa (Willd.) DC. — ethnomedicinal use and new pharmacological, toxicological and botanical results (POA/TOA antagonism). Journal of Ethnopharmacology 64(1): 23–34. — PubMed: Keplinger Laus 1999
Allen-Hall L, Cano P, Arnason JT, et al. (2007). Treatment of THP-1 cells with Uncaria tomentosa extracts differentially regulates the expression of IL-1beta and TNF-alpha. Journal of Ethnopharmacology 109(2): 312–317. — PubMed: Allen-Hall 2007
Hardin SR (2007). Cat's claw: an Amazonian vine decreases inflammation in osteoarthritis. Complementary Therapies in Clinical Practice 13(1): 25–28. — PubMed: Hardin OA review 2007
Smolen JS, Landewé R, Bijlsma J, et al. (2020). EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2019 update. Annals of the Rheumatic Diseases 79(6): 685–699. — PubMed: EULAR 2019 RA guidelines
Singh JA, Saag KG, Bridges SL Jr, et al. (2016). 2015 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis & Rheumatology 68(1): 1–26. — PubMed: ACR 2015 RA guidelines
Setty AR, Sigal LH (2005). Herbal medications commonly used in the practice of rheumatology: mechanisms of action, efficacy, and side effects. Seminars in Arthritis and Rheumatism 34(6): 773–784. — PubMed: Setty Sigal herbal rheumatology review

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