At the 2026 ASCO Annual Meeting, Johnson & Johnson announced Phase 1b data for pasritamig, a KLK2/CD3 bispecific TCE, in combination with docetaxel for metastatic castration-resistant prostate cancer (mCRPC): the combination showed significant efficacy with a favorable safety profile and no cytokine release syndrome of any grade, and has advanced to Phase 3 clinical trials. KLK2 has transitioned from a “classic prostate cancer biomarker” to a next-generation immunotherapy star target, bringing the KLK family back into the research spotlight.
The human tissue kallikrein-related peptidase (KLK) family comprises 15 secreted serine proteases and forms the largest contiguous protease gene cluster in the human genome. Beyond prostate cancer, KLK family members play important roles in various diseases, including inflammatory skin disorders, neurological diseases, and ovarian cancer. This article systematically reviews the biological characteristics, disease associations, and research progress of the KLK family to provide a reference for researchers in related fields.
The human tissue kallikrein family consists of 15 secreted serine proteases (KLK1–KLK15), whose encoding genes are clustered on the long arm of chromosome 19 at 19q13.4, forming the largest contiguous protease gene cluster in the human genome. All KLKs are single-chain polypeptides, sharing approximately 40% sequence homology among family members, with KLK2 and KLK3 showing the highest homology (~80%) [1].
Taxonomically, KLKs belong to the S1 family of serine proteases (chymotrypsin-like), which includes approximately 80% of all known human serine proteases. In addition to tissue kallikreins, humans also have plasma kallikrein (KLKB1), encoded by the KLKB1 gene on chromosome 4, which does not belong to the KLK family [2].
Figure 1. Schematic representation of KLK family gene and protein structure
Source: Prassas I, et al. Nat Rev Drug Discov. 2015;14(12):832-846.
All KLKs are synthesized and secreted as zymogens (pro-KLKs), comprising an N-terminal signal peptide, a propeptide, and a mature protease domain. The signal peptide is cleaved during secretion, and the propeptide is removed extracellularly via proteolytic cleavage to generate the active form.
Activation cleavage typically occurs after basic amino acids (Lys or Arg) and is mediated by trypsin-like activity. Most KLKs can be activated by other KLKs, and some (such as KLK2, KLK5, KLK6, KLK13) are capable of autoactivation. The sole exception is KLK4, whose activation requires cleavage after Gln30, mediated by a metalloproteinase [2].
Structurally, KLKs exhibit a typical serine protease fold — two β-barrel domains interact to form the active site cleft, with the catalytic triad (His57-Asp102-Ser195, chymotrypsinogen numbering) located at the bottom of the cleft. KLK1–KLK3 feature a prominent 99-loop (also called the kallikrein loop) near the substrate binding site, a characteristic structural feature of the KLK family that participates in substrate specificity regulation and endogenous inhibitor binding.
The proteolytic activity of KLKs is tightly regulated at multiple levels:
| Regulatory Level | Regulatory Mechanism | Key Factors |
|---|---|---|
| Transcriptional | Hormonal regulation, DNA methylation, miRNA | Androgens, glucocorticoids, vitamin D [1] [3] |
| Post-translational | Glycosylation | N-glycosylation/O-glycosylation, affecting substrate binding and inhibitor interactions [4] |
| Zymogen activation | Cascade activation / autoactivation | KLK cascade network (tissue-specific) [5] |
| Activity inhibition | Endogenous protein inhibitors | LEKTI (skin), serpins, α2-macroglobulin, Zn²⁺ [2] [6] |
Among endogenous inhibitors, LEKTI (encoded by the SPINK5 gene) is a key regulator of KLK activity in the skin, controlling the activities of KLK5, KLK7, KLK14, and others through reversible and allosteric binding. Zn²⁺ ions are also important physiological inhibitors — in the prostate, high Zn²⁺ concentrations suppress KLK activity; after ejaculation, Zn²⁺ transfers from KLK to semenogelins, releasing active KLKs and liquefying the seminal clot [2].
| Target | Primary Tissue Distribution | Major Disease Associations |
|---|---|---|
| KLK1 | Kidney, pancreas, salivary glands, prostate | Acute ischemic stroke, hypertension, asthma |
| KLK2 | Prostate | Prostate cancer |
| KLK3 | Prostate | Prostate cancer |
| KLK4 | Prostate, teeth | Prostate cancer, enamel formation |
| KLK5 | Skin, breast, brain | Netherton syndrome, atopic dermatitis |
| KLK6 | Brain, ovary, breast | Multiple sclerosis, Alzheimer’s disease, ovarian cancer |
| KLK7 | Skin, esophagus, kidney | Netherton syndrome, atopic dermatitis, colon cancer |
| KLK8 | Skin, brain, ovary | Psoriasis, neural plasticity, ovarian cancer |
| KLK9 | Thymus, testis | Breast cancer, ovarian cancer |
| KLK10 | Breast, prostate, ovary | Breast cancer, ovarian cancer |
| KLK11 | Prostate, ovary, stomach | Ovarian cancer, gastric cancer |
| KLK12 | Salivary glands, stomach | Less studied, angiogenesis |
| KLK13 | Thyroid, breast, prostate | Thyroid cancer, liver cancer |
| KLK14 | Skin, prostate, breast | Netherton syndrome, prostate cancer, renal cancer |
| KLK15 | Prostate, thyroid | Prostate cancer, renal cancer |
Prostate cancer is the most extensively studied disease area for the KLK family. From the decades-long clinical application of KLK3 (PSA) as the “gold standard” biomarker to the recent transformation of KLK2 from biomarker to therapeutic target, the KLK family has consistently been one of the core target groups in prostate cancer research.
KLK2 (human glandular kallikrein) shares approximately 80% amino acid homology with KLK3 (PSA), and their genes are located only ~12 kb apart in the 19q13.4 region [1]. Traditionally, KLK2 was considered a secreted protease whose primary function is to activate pro-KLK3 (PSA) and participate in semen liquefaction.
In 2025, Shen et al. published a study in Clinical Cancer Research that, for the first time, demonstrated KLK2 expression on the surface of prostate cancer cells: using FACS and confocal microscopy, the researchers detected KLK2 signals on the cell membrane in prostate cancer cell lines and patient-derived tumors [7]. This finding changed the traditional view of KLK as a purely secreted protease and provided key structural biology support for the development of antibody-based drugs targeting KLK2.
Drug Pipeline Progress:
| Drug Name | Target | Indication | Modality | Stage | Company |
|---|---|---|---|---|---|
| Pasritamig | KLK2×CD3 | Prostate cancer | Bispecific TCE | Phase 3 | Johnson & Johnson |
| Ac-225-labeled anti-KLK2 antibody | KLK2 | Prostate cancer | Radioimmunotherapy | Phase 1 | Johnson & Johnson |
| JNJ-75229414 | KLK2 | Prostate cancer | CAR-T | Phase 1 | Johnson & Johnson |
| JNJ-98768111 | KLK2 | Prostate cancer | ADC | Phase 1 | Johnson & Johnson |
Pasritamig is a first-in-class KLK2-targeted bispecific antibody whose differentiated advantage lies in the high tissue specificity of KLK2 — KLK2 is almost exclusively expressed in prostate tissue, with very low expression in other tissues, which significantly reduces the risk of off-target toxicity compared to PSMA-targeted agents (PSMA is expressed in salivary glands, kidneys, and nervous tissue, often causing adverse effects such as dry mouth) [11].
KLK3 encodes prostate-specific antigen (PSA), the “gold standard” clinical biomarker for prostate cancer screening, with chymotrypsin-like specificity. The classic function of PSA is to hydrolyze semenogelins I/II and fibronectin, leading to liquefaction of the seminal clot and release of sperm [2].
For a long time, KLK3/PSA was primarily used as a diagnostic biomarker. In recent years, with deeper understanding of its biological functions, KLK3 has been gradually transitioning from biomarker to therapeutic target:
Drug Pipeline Progress:
| Drug Name | Target | Indication | Modality | Stage | Company |
|---|---|---|---|---|---|
| Afala | KLK3 | Prostate cancer | Monoclonal antibody | Approved (2014) | Materia Medica Holding |
| RAD 402 | KLK3 | Prostate cancer | Antibody-conjugated radionuclide | Phase 1/2 | Radiopharm Theranostics |
| HB-300 | ACP3×KLK3 | Prostate cancer | Recombinant vector vaccine | Phase 1/2 | HOOKIPA Pharma |
RAD 402 (NCT07259213) dosed its first patient in March 2026 and represents a representative advance in KLK3-targeted radioligand therapy [12]. Therapeutic cancer vaccines (such as HB-300) use viral vectors to express PSA antigen in vivo, eliciting CTL responses to kill PSA-positive prostate cancer cells [13].
Since KLK2 and KLK3 share 80% amino acid homology and PSA circulates at high concentrations in the blood, the risk of cross-reactivity is an unavoidable concern when developing KLK2-targeted antibodies. Studies have shown that the high homology between KLK2 and KLK3 leads to a significantly higher probability of antibody cross-binding compared to other family members, so cross-reactivity testing against KLK3 requires special attention during antibody screening and specificity evaluation [7].
Unlike other KLKs (which are all secreted extracellular proteins), KLK4 is primarily localized to the nucleus. The full-length hK4-254 is cytoplasmic, while the N-terminally truncated hK4-205 is nuclear. Nuclear-localized KLK4 promotes prostate cancer cell proliferation by regulating transcription factors such as p21 and cyclin D1 [14].
This property means KLK4 is not suitable as a cell surface target for antibody drugs; currently, only early-stage explorations exist with cell therapies such as TCR-T [15].
Figure 2. Multiple mechanisms by which the KLK family remodels the tumor microenvironment. KLKs regulate tumor cell–microenvironment interactions through degrading ECM proteins, cleaving cell adhesion molecules, releasing ECM-bound growth factors, and activating other proteases.
Source: Srinivasan S, et al. Nat Rev Cancer. 2022.
The stratum corneum of the skin is another hot area of KLK family research. In the epidermis, KLK5, KLK7, and KLK14 form a precisely regulated proteolytic cascade network responsible for normal stratum corneum desquamation. When this cascade becomes dysregulated, it leads to a range of inflammatory skin diseases.
In normal skin, during differentiation, keratinocytes secrete inactive pro-KLKs into the intercellular spaces of the stratum corneum via lamellar bodies (LGs). These zymogens form an activation cascade:
Figure 3. Schematic representation of the skin epidermal KLK proteolytic cascade
Source: Prassas I, et al. Nat Rev Drug Discov. 2015.
KLK5 is the initiator of the cascade — proKLK5 possesses autoactivation capacity and can convert itself to the active form, subsequently cleaving and activating proKLK7, proKLK8, and proKLK14. Active KLK14 can in turn activate proKLK5, creating a positive feedback loop that amplifies the proteolytic cascade. Activated KLK5, KLK7, and KLK14 ultimately degrade corneodesmosomal proteins (DSG1, DSC1, CDSN), leading to breakdown of intercellular connections between corneocytes and normal desquamation [16].
The activity of this cascade is finely regulated by multiple factors. Within the epidermis, there exist pH and calcium gradients: the calcium gradient controls the formation and secretion of lamellar bodies — through which KLK zymogens are released into the stratum corneum [36]; while the pH gradient regulates activity levels by influencing the binding of KLKs to endogenous inhibitors such as LEKTI [17]. The LEKTI protein, encoded by the SPINK5 gene, is the most critical endogenous inhibitor of KLK activity in the skin, regulating the activity of the entire cascade through reversible and allosteric binding [6].
Netherton syndrome (NS) is a rare inherited skin disease caused by loss-of-function mutations in the SPINK5 gene, leading to defective or absent LEKTI protein. Loss of LEKTI results in uncontrolled activation of KLK5 and downstream KLKs, causing excessive degradation of desmosomal proteins and severe impairment of the epidermal barrier [18].
NS patients present with congenital ichthyosiform erythroderma, bamboo hair (trichorrhexis invaginata), and atopic diathesis (allergic rhinitis, asthma, food allergies, etc.). Severe cases can be life-threatening due to infections and electrolyte disturbances. The incidence of NS is approximately 1 in 200,000 newborns.
Gene knockout studies have shown that in Spink5-deficient mice, simultaneous knockout of KLK5 and KLK7 can fully rescue the lethal phenotype [19]. This indicates that KLK5 is the core driver in the pathogenesis of NS, and inhibiting KLK5 is a key therapeutic strategy for NS.
In lesions of patients with atopic dermatitis (AD), multiple KLKs (such as KLK5, KLK7, KLK14, etc.) are upregulated [20]. Increased KLK activity leads to abnormal epidermal barrier function, while simultaneously promoting inflammation through activation of protease-activated receptor 2 (PAR2), inducing the release of pro-inflammatory cytokines such as thymic stromal lymphopoietin (TSLP) [21].
AD is a chronic inflammatory skin disease affecting approximately 20% of children and 10% of adults globally, with a huge market size (dupilumab sales exceeded $10 billion in 2023). KLK5/7-targeted drugs offer a differentiated therapeutic mechanism for AD.
Drug Pipeline Progress:
| Drug Name | Target | Indication | Modality | Stage | Company |
|---|---|---|---|---|---|
| TRIV-509 | KLK5×KLK7 | Atopic dermatitis, asthma | Bispecific antibody | Phase 2 | Triveni Bio |
| SXR-1096 | KLK5×KLK7×KLK14 | Netherton syndrome | Small-molecule inhibitor | Phase 1/2 | Sixera Pharma |
| BCX-17725 | KLK5 | Netherton syndrome | Fusion protein | Phase 1 | BioCryst |
| DS-2325 | KLK5 | Netherton syndrome | Gene therapy | Phase 1 | Daiichi Sankyo |
| ATR-12 | KLK5 | Netherton syndrome | Engineered bacteria | Phase 1 | Azitra |
TRIV-509 is the most advanced bispecific antibody in the KLK field. It has shown superior efficacy compared to IL-4R inhibitors (dupilumab) in multiple preclinical AD models and demonstrated rapid improvement in skin biopsy samples from AD patients [22]. Phase II clinical trials are currently underway.
The role of the KLK family in the nervous system is equally important. KLK1, KLK6, and KLK8 are the three most extensively studied members in the brain, involved in stroke neuroprotection, demyelinating diseases, and neural plasticity, respectively.
KLK1 (tissue kallikrein) is the earliest discovered and most extensively studied member of the KLK family. Its classic function is to catalyze the release of kinins (bradykinin and kallidin) from kininogens, participating in blood pressure regulation, inflammatory responses, and tissue repair through the kinin B2 receptor signaling pathway [23].
In acute ischemic stroke (AIS), KLK1 has well-documented neuroprotective effects, improving cerebral blood flow, reducing infarct volume, and promoting neurological recovery [24].
Drug Pipeline Progress:
| Drug Name | Target | Indication | Modality | Stage | Company |
|---|---|---|---|---|---|
| DM199 | KLK1 | Acute ischemic stroke | Recombinant protein | Phase 2/3 | DiaMedica |
| PTH-0366 | KLK1 | Acute ischemic stroke | Recombinant protein | Phase 1 | Protheragen |
DM199 (recombinant human tissue kallikrein 1) has entered a global multicenter Phase II/III clinical trial (NCT05065216), enrolling patients at over 100 research centers worldwide [25].
KLK6 (also known as Neurosin, Zyme) is one of the most abundant KLKs in the brain and spinal cord. It is synthesized de novo by reactive astrocytes and is a molecular trigger of reactive astrogliosis.
KLK6 is closely associated with inflammatory demyelination in multiple sclerosis (MS) lesions. Inhibition of KLK6 delays symptom onset in experimental autoimmune encephalomyelitis (EAE). In Alzheimer’s disease, KLK6 participates in amyloid metabolism and may affect the production and clearance of Aβ [26].
Currently, KLK6-targeted drugs are still in the preclinical stage, including engineered protein inhibitors, small-molecule inhibitors, and covalent probes [27].
KLK8 (also known as Neuropsin) is a key regulator of neural plasticity. It is highly expressed in the hippocampus and participates in synaptic remodeling during learning and memory. KLK8 cleaves extracellular matrix proteins and neural cell adhesion molecules to regulate synaptic plasticity [28].
In the skin, KLK8 is significantly upregulated in psoriatic lesions, and serum KLK8 levels correlate with disease severity. KLK8 participates in the formation of psoriatic lesions, playing a particularly key role in the development of neutrophil microabscesses, but its mechanism of action differs from that of classic desquamatory KLKs [29].
Beyond the three main research areas outlined above, multiple KLK family members hold significant value as biomarkers in various cancers:
KLK6, KLK10, KLK11, and others are aberrantly expressed in ovarian cancer and serve as diagnostic and prognostic biomarkers. KLK6 is elevated in the ascites of patients with peritoneal metastasis and can be used to differentiate benign from malignant ascites [30]. KLK11 can distinguish ovarian cancer from healthy controls and is suitable for longitudinal screening [31].
KLK10 acts as a tumor suppressor in breast cancer, where promoter methylation leads to silencing of expression, associated with poor prognosis [32]. KLK6 promotes breast cancer cell invasion and is associated with metastasis [30].
KLK6 and KLK7 are significantly upregulated in colon cancer. KLK7 promotes invasion and peritoneal dissemination of colorectal cancer cells and exhibits high diagnostic efficacy [33]. KLK10 plays an oncogenic role in colon cancer with significantly elevated expression [30].
KLK13 is aberrantly expressed in thyroid cancer and has potential as a diagnostic biomarker [30]. KLK15 is upregulated in prostate cancer, associated with tumor aggressiveness, and can serve as a prognostic indicator [35].
To support KLK family-related research, CUSABIO provides the following recombinant proteins, ELISA kits, and antibody products:
| Target | Code | Product Name | Source |
|---|---|---|---|
| KLK1 | CSB-EP012446HU | Recombinant Human Kallikrein-1 (KLK1) | E.coli |
| KLK10 | CSB-EP012447HU1 | Recombinant Human Kallikrein-10 (KLK10), partial | E.coli |
| KLK2 | CSB-EP012453HU | Recombinant Human Kallikrein-2 (KLK2) | E.coli |
| KLK7 | CSB-EP012458HU | Recombinant Human Kallikrein-7 (KLK7), partial | E.coli |
| Klk7 | CSB-EP012458RA | Recombinant Rat Glandular kallikrein-7, submandibular/renal (Klk7) | E.coli |
| Klk1b22 | CSB-EP325391MO | Recombinant Mouse Kallikrein 1-related peptidase b22 (Klk1b22) | E.coli |
| Klk8 | CSB-EP720268MO | Recombinant Mouse Kallikrein-8 (Klk8) | E.coli |
| Klk14 | CSB-EP806542MO | Recombinant Mouse Kallikrein-14 (Klk14) | E.coli |
| Klk14 | CSB-EP806542MOa2 | Recombinant Mouse Kallikrein-14 (Klk14) | E.coli |
| KLK7 | CSB-YP012458HU | Recombinant Human Kallikrein-7 (KLK7), partial | Yeast |
| Klk8 | CSB-YP720268MO | Recombinant Mouse Kallikrein-8 (Klk8) | Yeast |
| Klk14 | CSB-YP806542MO | Recombinant Mouse Kallikrein-14 (Klk14) | Yeast |
| KLK9 | CSB-MP892334HU | Recombinant Human Kallikrein-9 (KLK9) | Mammalian cell |
| KLK15 | CSB-MP752074SWB | Recombinant Saguinus oedipus Kallikrein-15 (KLK15) | Mammalian cell |
| KLK9 | CSB-EP892334HU | Recombinant Human Kallikrein-9 (KLK9) | E.coli |
| KLK12 | CSB-EP892137HU | Recombinant Human Kallikrein-12 (KLK12) | E.coli |
| KLK7 | CSB-EP012458HU1 | Recombinant Human Kallikrein-7 (KLK7), partial | E.coli |
| Klk1b5 | CSB-EP325792MO | Recombinant Mouse Kallikrein 1-related peptidase b5 (Klk1b5) | E.coli |
| KLK3 | CSB-EP012454MOW | Recombinant Macaca mulatta Prostate-specific antigen (KLK3) | E.coli |
| KLK2 | CSB-YP012453HU | Recombinant Human Kallikrein-2 (KLK2) | Yeast |
| Target | Code | Product Name | Tested Applications |
|---|---|---|---|
| KLK3 | CSB-RA548583A0HU | KLK3 Recombinant Monoclonal Antibody | ELISA, IHC; Recommended dilution: IHC:1:50-1:200 |
| KLK5 | CSB-RA729707A0HU | KLK5 Recombinant Monoclonal Antibody | ELISA, WB, IHC, FC; Recommended dilution: WB:1:500-1:5000, IHC:1:50-1:200, FC:1:20-1:200 |
| KLK2 | CSB-RA012453MA1HU | KLK2 Recombinant Monoclonal Antibody | ELISA; Recommended dilution: ELISA:1:1000-1:10000 |
| KLK11 | CSB-PA000045 | Cleaved-KLK11 (I54) Antibody | WB, ELISA; WB:1:500-1:2000, ELISA:1:10000 |
| KLK8 | CSB-PA000046 | Cleaved-KLK8 (V33) Antibody | WB, ELISA; WB:1:500-1:2000, ELISA:1:10000 |
| KLK1 | CSB-PA005798 | KLK1 Antibody | WB, ELISA; WB:1:500-1:2000, ELISA:1:20000 |
| KLK3 | CSB-PA006113 | KLK3 Antibody | WB, ELISA; WB:1:500-1:2000, ELISA:1:10000 |
| KLK3 | CSB-PA009525 | KLK3 Antibody | WB, IHC, IF, ELISA; WB:1:500-1:2000, IHC:1:100-1:300, IF:1:200-1:1000, ELISA:1:20000 |
| KLK1 | CSB-PA012446GA01HU | KLK1 Antibody | ELISA, WB, IHC |
| KLK11 | CSB-PA012448GA01HU | KLK11 Antibody | ELISA, IHC |
| KLK5 | CSB-PA012456GA01HU | KLK5 Antibody | ELISA |
| KLK8 | CSB-PA012459GA01HU | KLK8 Antibody | ELISA, WB |
| KLK3 | CSB-PA012454GA01HU | KLK3 Antibody | ELISA, IHC |
| KLK3 | CSB-PA920807 | KLK3 Antibody | ELISA, IHC; ELISA:1:500-1:2000, IHC:1:5-1:20 |
| KLK3 | CSB-PA554992 | KLK3 Antibody | ELISA, IHC; ELISA:1:500-1:2000, IHC:1:10-1:25 |
| KLK1 | CSB-PA086611 | KLK1 Antibody | ELISA, IHC; ELISA:1:1000-1:5000, IHC:1:50-1:200 |
| KLK1 | CSB-PA248038 | KLK1 Antibody | ELISA, IHC; ELISA:1:1000-1:5000, IHC:1:50-1:200 |
| KLK4 | CSB-PA211882 | KLK4 Antibody | ELISA, IHC; ELISA:1:2000-1:5000, IHC:1:25-1:100 |
| KLK4 | CSB-PA214768 | KLK4 Antibody | ELISA, IHC; ELISA:1:2000-1:5000, IHC:1:25-1:100 |
| KLK7 | CSB-PA094965 | KLK7 Antibody | ELISA, IHC; ELISA:1:1000-1:5000, IHC:1:25-1:100 |
| Target | Code | Product Name | Detection Range | Sensitivity |
|---|---|---|---|---|
| KLK3 | CSB-E08276m | Mouse Kallikrein 1-related peptidase b3,Klk3 ELISA Kit | 0.312 ng/mL-20 ng/mL | 0.078 ng/mL |
| KLK6 | CSB-E09248h | Human Kallikrein 6,KLK 6 ELISA Kit | 1.25 ng/ml-80 ng/ml | 0.31 ng/mL |
| KLK10 | CSB-E10095h | Human Kallikrein 10,KLK 10 ELISA Kit | 1.675 ng/mL-40 ng/mL | 0.7 ng/mL |
| KLK1 | CSB-E11437h | Human Kallikrein 1,KLK 1 ELISA Kit | 0.78 ng/mL-50 ng/mL | 0.195 ng/mL |
| KLK2 | CSB-E13094h | Human Kallikrein 2(hK 2) ELISA Kit | 62.5 pg/mL-4000 pg/mL | 15.6 pg/mL |
| KLK7 | CSB-E13797h | Human Kallikrein 7,KLK 7 ELISA Kit | 0.625 ng/mL-40 ng/mL | 0.156 ng/mL |
| KLK14 | CSB-EL012451HU | Human Kallikrein-14(KLK14) ELISA kit | 1.56 ng/ml-100 ng/ml | 0.39 ng/ml |
| KLK4 | CSB-EL012455HU | Human Kallikrein-4(KLK4) ELISA kit | 0.156 ng/mL-10 ng/mL | 0.039 ng/mL |
| KLK5 | CSB-EL012456HU | Human Kallikrein-5(KLK5) ELISA kit | 62.5 pg/mL-4000 pg/mL | 15.6 pg/mL |
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